AIM: To investigate the effects of allicin on both telomeraseactivity and apoptosis in gastric cancer SGC-7901 cells.METHODS: The gastric cancer SGC-7901 adenocarcinomacells were treated with allicin and the cell cycl...AIM: To investigate the effects of allicin on both telomeraseactivity and apoptosis in gastric cancer SGC-7901 cells.METHODS: The gastric cancer SGC-7901 adenocarcinomacells were treated with allicin and the cell cycle, inhibitoryrate, apoptosis, telomerase activity and morphologic changeswere studied by MTT assay, flow cytometry (FCM), TRAP-PCR-ELISA assay, light microscope, electron microscoperespectively. Results were compared with that of AZT (3′-Azido-3′-deoxythymidine).RESULTS: SGC-7901 cells were suppressed after exposureto allicin of 0.016 mg/ml, 0.05 mg/ml, and 0.1 mg/mi for48 h. Compared with the control, the difference wassignificant (P＜0.05). Allicin could induce apoptosis of thecells in a dose-dependent and non-linear manner andincrease the proportion of cells in the G2/M phase. Comparedwith the control, the difference was significant in terms ofthe percentage of cells in the G2/M phase (P＜0.05). Allicincould inhibit telomerase activity in a time-dependent anddose-dependent pattern. After exposure to allicin at 0.016mg/ml for 24 hours, SGC-7901 cells showed typicalmorphologic change.CONCLUSION: Allicin can inhibit telomerase activity andinduce apoptosis of gastric cancer SGC-7901 cells. Allicinmay be more effective than AZT.展开更多
AIM: To study the inhibitory effects of a Shuangling Fuzheng anticancer preparation (SFAP) on the human gastric cancer cell line SGC-7901 in vitro as well as its immune-modulated effects in a cyclophosphamide-treated ...AIM: To study the inhibitory effects of a Shuangling Fuzheng anticancer preparation (SFAP) on the human gastric cancer cell line SGC-7901 in vitro as well as its immune-modulated effects in a cyclophosphamide-treated murine model. METHODS: MTT experiments and immunocytochemistry ABC experiments were performed for detecting the proliferation of SGC-7901 cells in vitro and protein expression of c-myc. The staphylococcal protein A (SPA) rosette test was utilized for measuring the ratio of T-lymphocyte subsets from peripheral blood in a cyclophosphamide-treated murine model. Enzyme- linked immunosorbant assay (ELISA) was performed for measuring the levels of serum sIL-2R in treated mice, while immunoturbidimetry was used for measuring the levels of immunoglobulins (Ig). RESULTS: SFAP (40-640 mg/L, 48 h) inhibited the proliferation of SGC-7901 cells, and a positive correlation was noted between inhibitory effects and dosage. At a dosage of 160-320 mg/L in cultured cells, the expression of c-myc was decreased. SFAP (50-200 mg/kg) increased the percentage of CD3+ and CD4+ T-lymphocytes, the ratio of CD4/CD8, and the contents of Ig such as IgM, IgG or IgA, but decreased the levels of serum sIL-2R in peripheral blood from cyclophosphamide-treated mice. CONCLUSION: SFAP can inhibit the proliferation of SGC-7901 cells via the c-myc gene. In addition, SFAP can modulat the cellular and humoral immunity in cyclophosphamide-induced immunosuppressed mice.展开更多
AIM：Toinvestigate the effects of vitamin E succinate(VES)on the expression of c-jun gene and protein in human gastric cancer SGC-7901 cells.METHODS:After SGC-7901cells were treated with VESat different doses(5,10,20m...AIM：Toinvestigate the effects of vitamin E succinate(VES)on the expression of c-jun gene and protein in human gastric cancer SGC-7901 cells.METHODS:After SGC-7901cells were treated with VESat different doses(5,10,20mg·L^-1)at different time,reverse transcription-PCR technique was used to detect the level of c-jun mRNA;Western Blot was applied to measure the expression of c-jun protein.RESULTS:After the cells were theated with VESat 20mg·L^-1for 3h,the expression rapidly reached its maximun that was3.5times of UT control(P<0.01).The level of c-jun mRNA was also increased following treatment of VESfor 6h.However the expression after treatment of VES at 5mg·L^-1for24h was 1.6tmes compared with UTcontrol(P<0.01),Western blot analysis showed that the level of c-jun protein was obviusly elevated in VES-treated SGC-7901cells at 20mg·L^-1for3h,The expression of c-jun protein was gradually increased after treatment of VES at 20mg·L^-1for3,6,12and24h,respectively,with an evident time-effect relationship.CONCONCLUSION:The levels of c-jun mRNA and protein in VES-treated SGC-7901cells were increased in a dose-and time-dependent manner;the expression of c-jun was prolonged by VES,indicating that c-jun is involvedin VES-induced apoptosis in SGC-7901 cells.展开更多
AIM: To investigate the effects of mitomycin (MMC)combined with sulindac on cell viability, apoptotic induction and expression of apoptosis-related gene Bcl-2 and cyclooxygenase-2 (COX-2)in gastric cancer SGC-7901cell...AIM: To investigate the effects of mitomycin (MMC)combined with sulindac on cell viability, apoptotic induction and expression of apoptosis-related gene Bcl-2 and cyclooxygenase-2 (COX-2)in gastric cancer SGC-7901cells.METHODS: Human gastric cancer SGC-7901 cells were divided into three treatment groups,namely sulindac treatment group, MMC treatment group and combined sulindac with MMC treatment group. After being treated with drugs, cell viability was examined by MTr assay.Flow cytometry was used to evaluate the cell cycle distribution and apoptotic rates. Morphology of the cells was observed under light microscope and interactive laser microscope. Expression of COX-2 and Bcl-2 was determined by immunocytochemical method.RESULTS: After exposure for 12 h to three kinds of drugs,gastric cancer SGC-7901 cells presented some morphological features of apoptosis, including cell shrinkage, nuclear condensation, DNA fragmentation and formation of apoptotic bodies. Growth inhibition was more obvious in combined sulindac with MMC treatment group and sulindac treatment group than in MMC treatment group. The apoptotic rates in co-treated cells and MMC-treated cells 24 h after treatment were 12.0% and 7.2%, respectively.After exposure for 24 h to MMC, the expression of COX-2and Bcl-2 protein was up-regulated, COX-2 levels were down-regulated but Bcl-2 gene expression was not changed significantly in combined treatment group.CONCLUSION: MMC-induced apoptosis is reduced by up-regulating the expression of COX-2 and Bcl-2 genes.MMC combined with sulindac can suppress the growth of gastric cancer cells through induction of apoptosis mediated by down-regulation of apoptosis-related Bcl-2and COX-2 gene.展开更多
AIM: To study the moleucle action mechunisms of NM-3 on the growth of human gastric cancer SGC-7901 cells in vivo or in vitro.METHODS: SGC-7901 from human non-differentiated gastric cancer cell line was cultured with ...AIM: To study the moleucle action mechunisms of NM-3 on the growth of human gastric cancer SGC-7901 cells in vivo or in vitro.METHODS: SGC-7901 from human non-differentiated gastric cancer cell line was cultured with NM-3 at 100 mg/ml for 24 h. We observed its inhibitory rate and the density of micro-vascular growth in grafted mice with human gastric cancer SGC-7901. The apoptosis of human gastric cancer SGC-7901 was revealed in NM-3 treatment group by using terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-fluorescene nick end labeling (TUNEL)method and flow cytometry analysis.RESULTS: The growth of SGC-7901 cells was markedly inhibited compared with control growp, which was smaller than that in normal saline control group (4.17 g±0.22 g VS 9.45 g±1.38 g, P＜0.01). The level of apoptosis of human gastric cell line SGC-7901 was obviously increased in NM-3treatment group at 1 mg.L-1 for 24 h. NM-3 inducing apoptotic index in NM-3 plus carboplatin group was 3.5 times that of carboplatin control group (TUNEL: 27.98±6.12 % VS 12.94±2.12 %, FACScan: 26.86±5.69 % VS11.86±1.09 %,P＜0.01). Western blot analysis showed that the apoptotic index of human gastric cancer was elevated for 12, 24 and 36 h with an evident time-effect relationship in groups at 100 mg.L-L. NM-3 enhanced the inhibitive effects and sensitivity of chemotherapy for human gastric cancer in nude mice. These results suggested that NM-3 played a key inhibitive role in the growth of grafted human gastric cancer in nude mice.CONCLUSION: NM-3 can inhibit the growth of human gastric cancer cell line SGC-7901, and enhance the sensitivity of carboplatin on SGC-7901 and induced its apoptosis.展开更多
[Objectives]To observe the effect of drug-containing serum from different extracts of Phyllanthus reticulatus leaf on the proliferation of human gastric cancer SGC-7901 cells and the effect of in vivo on the life exte...[Objectives]To observe the effect of drug-containing serum from different extracts of Phyllanthus reticulatus leaf on the proliferation of human gastric cancer SGC-7901 cells and the effect of in vivo on the life extension rate of mice with H22 ascites tumor,and to investigate the effects of chemical components such as Corilagin,ethyl gallate,ethyl brevifolincarboxylate,and gallic acid on the proliferation of human gastric cancer SGC-7901 cells.[Methods]MTT method was used to observe the inhibitory effect of drug-containing serum of different extracts of P.reticulatus leaf on human gastric cancer SGC-7901 cells in vitro to determine its active site.The active site was used as the research object to establish a Kunming mouse ascites tumor model,to investigate the effect on the life extension rate of mice with H22 ascites tumor,to further separate the monomer components from the effective fraction and investigate its effect on human gastric cancer SGC-7901 cells.[Results]Compared with the 10%blank serum control group,10%drug-containing serum of ethyl acetate and n-butanol in P.reticulatus leaf had significant inhibitory effect on the proliferation of human gastric cancer SGC-7901 cells,and the inhibition rate was 34.99%and 28.68%,respectively(P<0.05).Compared with the blank group,the survival time of the high dose group of ethyl acetate in P.reticulatus leaf was significant(P<0.05).Gallic acid,Corilagin,and Brevifolincarboxylic acid ethyl ester had a significant inhibitory effect on the proliferation of human gastric cancer SGC-7901 cells,with IC 50 of 26.52,70.45,and 158.86μg/mL,respectively.Ethyl gallate had no inhibitory effect on the proliferation of human gastric cancer SGC-7901 cells,and its IC 50 was 251.96μg/mL.[Conclusions]The drug-containing serum of ethyl acetate and n-butanol extract of P.reticulatus can inhibit the proliferation of human gastric cancer SGC-7901 cells.Ethyl acetate of P.reticulatus leaves can increase the life extension rate of mice with H22 ascites tumor.Gallic acid,Corilagin,and Brevifolincarboxylic acid ethyl ester isolated from its active site are the material basis for inhibiting the proliferation of human gastric cancer SGC-7901 cells.展开更多
Objective: To investigate the cytotoxic effects and the potential mechanisms of crebanine N-oxide in SGC-7901 gastric adenocarcinoma cells. Methods: The cytotoxicity of crebanine N-oxide was evaluated by 3-(4,5-dimeth...Objective: To investigate the cytotoxic effects and the potential mechanisms of crebanine N-oxide in SGC-7901 gastric adenocarcinoma cells. Methods: The cytotoxicity of crebanine N-oxide was evaluated by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay and cellular morphology was observed under a microscope. Cell apoptosis was determined by flow cytometry using propidium iodide staining. The expression levels of apoptotic-related proteins, cleaved caspase-3, cytochrome C, p53 and Bax, and autophagyrelated proteins p62, beclin1 and LC3 were detected by Western blotting assays. Results: Crebanine N-oxide treatment significantly inhibited the proliferation of SGC-7901 cells in a dose-dependent and timedependent manner via induction of G2-phase cell cycle arrest, apoptosis, and autophagy in SGC-7901 cells.Conclusions: Crebanine N-oxide could inhibit the growth of gastric cancer cells by promoting apoptosis and autophagy and could be used as a potential agent for treating gastric cancer.展开更多
Objective： To investigate the effects of xanthotoxin from Apiaceae medicinal plants on cell proliferation and apoptosis, and explore its mechanism of action against human gastric carcinoma SGC-7901 cells in vitro.Met...Objective： To investigate the effects of xanthotoxin from Apiaceae medicinal plants on cell proliferation and apoptosis, and explore its mechanism of action against human gastric carcinoma SGC-7901 cells in vitro.Methods： SGC-7901, HepG-2, MCF-7, and A549 cells were treated with different concentrations of xanthotoxin（10, 20, 60, 80, 100, 120, 140, and 160 μg/mL） for 48 h, and the cell viability（IC50） was determined by MTT assay; Xanthotoxin-induced apoptosis in cells was observed by using Hoechst 33258 Staining Kit and Annexin V-FITC Apoptosis Detection Kit; Flow cytometry was used to detect apoptosis related proteins of Fas/FasL, Bid, and DR5/TRAIL proteins in human gastric carcinoma SGC-7901 cells after being treated by xanthotoxin; The influence of xanthotoxin on Caspase-8 protein expression in the cells was determined by Flouormetric Assay Kit.Results： Xanthotoxin obviously inhibited SGC-7901, HepG-2, MCF-7, and A549 cells proliferation, and its inhibition was in a concentration-dependent manner; flow cytometry results showed that in a certain concentration range, xanthotoxin can increase the expression levels of Fas/FasL and DR5/TRAIL proteins in a concentration-dependence manner. The content of Bid protein in cells was increased, and it showed concentration-dependence.Conclusion： Xanthotoxin may induce SGC-7901 cells apoptosis in a certain concentration range through the Fas/FasL protein mediated death receptor pathway, or by DR5/TRAIL mediated death receptor pathway, and increase the expression level of death receptor protein, activation Caspase-8, activating downstream effect factor, inducing cell apoptosis, or activate Caspase-8 cutting activate protein Bid, and then enter the mitochondrial pathway, induction of apoptosis.展开更多
AIM:To investigate the inhibitory effect of acetylshikonin on human gastric carcinoma cell line SGC-7901 and its mechanism. METHODS:MTT assay was used to assess the inhibitory effect of acetylshikonin on proliferation...AIM:To investigate the inhibitory effect of acetylshikonin on human gastric carcinoma cell line SGC-7901 and its mechanism. METHODS:MTT assay was used to assess the inhibitory effect of acetylshikonin on proliferation of SGC-7901 cells.Apopt osis-inducing effect was determined by flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling with Hoechst staining.Expression of mRNA and protein in Bcl-2 and Bax was analyzed by reverse transcription-polymerase chain reaction and Western blot.Antitumor effect of acetylshikonin on a mouse SGC-7901 model was also determined. RESULTS:Forty-eight hours after treatment with acetylshikonin,MTT assay showed that acetylshikonin inhibited the proliferation of SGC-7901 cells in a dose-dependent manner.The half maximal inhibitory concentration of acetylshikonin to SGC-7901 cells was 0.428±0.07 mg/L.Cell shrinkage,nuclear pyknosis and chromatin condensation,which are the characteristics of cell apoptosis,were observed in treated SGC-7901 cells and the percentage of apoptosis increased in a dose-dependent manner.Acetylshikonin downregulated the expression of Bcl-2 and up-regulated the expression of Bax in the treated SGC-7901 cells compared with the controls.The experiment in vivo showed that 0.5,1,and 2 mg/kg of acetylshikonin significantly inhibited the growth of tumor in the mouse SGC-7901 model,with an inhibitory rate of 25.00%-55.76%. CONCLUSION:Acetylshikonin inhibits the growth of SGC-7901 cells in vitro and in vivo by inducing cell apoptosis.展开更多
AIM:To investigate the effects of growth inhibition ofhuman gastric cancer SGC-7901 cell with RRR-α-tocopherylsuccinate(VES),a derivative of natural Vitamin E,viainducing apoptosis and DNA synthesis arrest.METHODS:Hu...AIM:To investigate the effects of growth inhibition ofhuman gastric cancer SGC-7901 cell with RRR-α-tocopherylsuccinate(VES),a derivative of natural Vitamin E,viainducing apoptosis and DNA synthesis arrest.METHODS:Human gastric cancer SGC-7901 cells wereregularly incubated in the presence of VES at 5,10 and20mg.L^(-1)(VES was dissolved in absolute ethanol anddiluted in RPMI 1640 complete condition mediacorrespondingly to a final concentration of VES and lmL.L^(-1)ethanol),succinic acid and ethanol equivalents asvehicle(VEH)control and condition-media only asuntreated(UT)control.Trypan blue dye exclusionanalysis and MTT assay were applied to detect the cellproliferation.37kBq of tritiated thymidine was added tocells and [~3H]TdR uptake was measured to observe DNAsynthesis.Apoptotic morphology was observed byelectron microscopy and DAPI staining.Flow cytometryand terminal deoxynucleotidyl transferase-mediated dUTPnick end labeling(TUNEL)assay were performed to detectVES-triggered apoptosis.RESULTS:VES inhibited SGC-7901 cell growth in a dose-dependent manner.The growth curve showed suppressionby 24.7%,49.2% and 68.7% following 24h of VEStreatment at 5,10 and 20 mg·L^(-1),respectively,similar tothe findings from MTT assay.DNA synthesis wasevidently reduced by 35%,45% and 98% after 24h VEStreatment at 20 mg·L^(-1)and 48h at 10 and 20 mg·L^(-1),respectively.VES induced SGC-7901 cells to undergoapoptosis with typically apoptotic characteristics,including morphological changes of.chromatincondensation,chromatincrescent formation/margination,nucleus fragmentation and apoptotic body formation,typical apoptotic sub-G1 peak by flow cytometry andincrease of apoptotic cells by TUNEL assay in which 90%of cells underwent apoptosis after 48h of VES treatment at20 mg·L^(-1).CONCLUSION:VES can inhibit human gastric cancer SGC-7901 cell growth by inducing apoptosis and DNA synthesisarrest,inhibition of SGC-7901 cell growth by VES is dose-and time-dependent.Therefore VES can function as apotent chemotherapeutic agent against human gastric carcinogenesis.展开更多
AIM: To determine the effect of apoptosis on gastric cancer cells (SGC-7901) induced by cis-9, trans-11-conjugated linoleic acid (c9, t11-CLA) and its possible mechanism in the inhibition of cancer cells growth.METHOD...AIM: To determine the effect of apoptosis on gastric cancer cells (SGC-7901) induced by cis-9, trans-11-conjugated linoleic acid (c9, t11-CLA) and its possible mechanism in the inhibition of cancer cells growth.METHODS: Using cell culture, flow cytometery and immunocytochemical techniques, we examined the cell growth, frequency of apoptosis and distribution of cell cycle,expression of ki67, bcl-2, Fas, and c-myc of SGC-7901 cells which were treated with various c9, t11-CLA concentrations (25,50,100 and 200 μmol@L-1) of c9, t11-CLA for 24h and 48 h,with a negative control (0.1% ethanol).RESULTS: The growth of SGC-7901 cells was inhibited by c9,t11-CLA. Eight days after treatment with various concentrations of c9,t11-CLA, as mentioned above, the inhibition rates were 5.9 %, 20.2 %,75.6 % and 82.4 %, respectively. The frequency of apoptosis on SGC-7901 cells induced by different concentrations of c9, t11-CLA (except for 25 μmol@L-1, 24 h) was significantly greater than that in the negative control (P＜0.01). To further investigate the influence of the cell cycle progression, we found that apoptosis induced by c9, t11-CLA may be involved in blocking the cell cycle of SGC-7901 cells. Immunocytochemical staining demonstrated that SGC-7901 cells preincubated in media supplemented with different c9, t11-CLA concentrations for various time periods significantly decreased the expressions of ki67 (the expression rates were 18.70-3.20 %, at 24 h and 8.10-0.20 % at 48 h, respectively), bd-2 (4.30-0.15 % at 24 h and 8.05 %-0 at 48 h),and c-myc(4.85-2.20 % at 24 h and 4.75-0.30 % at 48 h) as compared with those in the controls (the expressions of ki67, bcl-2, and c-mycwere 15.1% at 24 h and 13.5 % at 48 h, 6.80 % at 24 h and 8.00 % at 48 h,5.50 % at 24 h and 5.30 % at 48 h, respectively) (P＜0.01),whereas the expressions of Fas were increased (0.60-2.75 %,24 h and 0.45-5.95 %, 48 h).CONCLUSION: The growth and proliferation of SGC-7901 cells are inhibited by cg, t11-CLA via blocking the cell cycle,pathways of bcl-2-associated mitochondria with reduced expression of bcl-2 and Fas-associated death domain protein (FADD) with enhanced expression of Fas. But expression of c-myc on SGC-7901 cells is lower than that in negative control, which needs to be studied further.展开更多
AIM: To investigate the effect of c9, t1l-conjugated linoleic acid (c9, t11-CLA) on the invasion of human gastric carcinoma cell line and its possible mechanism of preventing metastasis.METHODS: Using reconstituted ba...AIM: To investigate the effect of c9, t1l-conjugated linoleic acid (c9, t11-CLA) on the invasion of human gastric carcinoma cell line and its possible mechanism of preventing metastasis.METHODS: Using reconstituted basement membrane invasion, chemotaxis, adhesion, PAGE substrate zymography and RT-PCR assays, we analyzed the abilities of invasion,direct migration, adhesion of intracellular matrix, as well as the activity of type IV collagenase and expression of tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 mRNA in SGC-7901 cells which were treated with gradually increased concentrations (25, 50, 100 and 200μmol/L) of c9,c11-CLA for 24 h.RESULTS: At the concentrations of 200μmol/L, 100μmol/L and 50μmol/L, c9,tll-CLA suppressed the invasion of SGC-7901 cells into the reconstituted basement membrane by 53.7 %, 40.9 % and 29.3 %, respectively, in comparison with the negative control. Only in the 200 μmol/L c9,tll-CLA group, the chemotaxis of SGC-7901 cells was inhibited by 16.0 % in comparision with the negative control. C9,tll-CLA also could inhibit the adhesion of SGC-7901 cells to laminin, fibronectin and Matrigel, increase the expression of TIMP-1 and TIMP-2 mRNA, and reduce type IV collegenase activities in the serum-free medium supernatant of SGC-7901 cells.CONCLUSION: c9,t11-C:LA can inhibit the invasion of SGC-7901 cells at multiple procedures in tumor metastasis cascade, which may be associated with the induction of TIMP-1 and TIMP-2 mRNA expression.展开更多
AIM: To evaluate the effects of tributyrin, a pro-drug of natural butyrate and a neutral short-chain fatty acid triglyceride, on the growth inhibition of human gastric cancer SGC-7901 cell.METHODS: Human gastric cance...AIM: To evaluate the effects of tributyrin, a pro-drug of natural butyrate and a neutral short-chain fatty acid triglyceride, on the growth inhibition of human gastric cancer SGC-7901 cell.METHODS: Human gastric cancer SGC-7901 cells were exposed to tributyrin at 0.5, 1, 2, 5, 10 and 50 mmol·L-^1 for 24-72h. MTT assay was applied to detect the cell proliferation.[^3H]-TdR uptake was measured to determine DNA synthesis.Apoptotic morphology was observed by electron microscopy and Hoechst-33258 staining. Flow cytometry and terminal deoxynudeotidyl transferase-mediated dUTP nick end labeling(TUNEL) assay were performed to detect tributyrin-triggered apoptosis. The expressions of PARP, Bcl-2 and Bax were examined by Western blot assay.RESULTS: Tributyrin could initiate growth inhibition of SGC-7901 cell in a dose-and time-dependent manner. [^3H]-TdR uptake by SGC-7901 cells was reduced to 33.6% after 48h treatment with 2mmol·L^-1 tributyrin, compared with the control (P<0.05). Apoptotic morphology was dell:ted by TUNEL assay. Flow cytometry revealed that tributyrin could induce apoptosis of SGC-7901 cells in dose-dependent manner. After 48 hours incubation with tributyrin at 2mmol·L^-1, the level of Bcl-2 protein was lowered, and the level of Bax protein was increased in SGC-7901, accompanied by PARP cleavage.CONCLUSION: Tributyrin could inhibit the growth of gastric cancer cells effectively in vitro by inhibiting DNA synthesis and inducing apoptosis, which was associated with the downregulated Bcl-2 expression and the up-regulated Bax expression. Therefore, tribublrin might be a promising chemopreventive and chemotherapeutic agent against human gastric carcinogenesis.展开更多
AIM: To explore the effects of mifepristone, a progesterone receptor (PR) antagonist, on the proliferation of human gastric adenocarcinoma cell line SGC-7 901 in vitro and the possible mechanisms involved.METHODS: In ...AIM: To explore the effects of mifepristone, a progesterone receptor (PR) antagonist, on the proliferation of human gastric adenocarcinoma cell line SGC-7 901 in vitro and the possible mechanisms involved.METHODS: In situ hybridization was used to detect the expression of PR mRNA in SGC-7 901 cells. After treatment with various concentrations of mifepristone (2.5, 5, 10,20μmol/L) at various time intervals, the ultrastructural changes, cell proliferation, cell-cycle phase distribution, and the expression of caspase-3 and Bcl-XL were analyzed using transmission electron microscopy (TEM), tetrazolium blue (MTT) assay, ^3H-TdR incorporation, flow cytometry, and reverse transcription-polymerase chain reaction (RT-PCR).RESULTS: Mifepristone markedly induced apoptosis and inhibited cell proliferation of PR- positive SGC-7 901 cells revealed by TEM, MTT assay and ^3H-TdR incorporation, in a dose- and time-dependent manner. The inhibitory rate was increased from 8.98% to 51.29%. Flow cytometric analysis showed mifepristone dose-dependently decreased cells in S and G2/M phases, increased cells in G0/G1 phase,reduced the proliferative index from 57.75% to 22.83%.In addition, mifepristone up-regulated the expression of caspase-3, and down- regulated the Bcl-XL expression,dose-dependently.CONCLUSION: Mifepristone effectively inhibited the proliferation of PR-positive human gastric adenocarcinoma cell line SGC-7 901 in vilrothrough multiple mechanisms, and may be a beneficial agent against human adenocarcinoma.展开更多
基金the Natural Science Foundation of Jiangsu,Province No.BJ98110
文摘AIM: To investigate the effects of allicin on both telomeraseactivity and apoptosis in gastric cancer SGC-7901 cells.METHODS: The gastric cancer SGC-7901 adenocarcinomacells were treated with allicin and the cell cycle, inhibitoryrate, apoptosis, telomerase activity and morphologic changeswere studied by MTT assay, flow cytometry (FCM), TRAP-PCR-ELISA assay, light microscope, electron microscoperespectively. Results were compared with that of AZT (3′-Azido-3′-deoxythymidine).RESULTS: SGC-7901 cells were suppressed after exposureto allicin of 0.016 mg/ml, 0.05 mg/ml, and 0.1 mg/mi for48 h. Compared with the control, the difference wassignificant (P＜0.05). Allicin could induce apoptosis of thecells in a dose-dependent and non-linear manner andincrease the proportion of cells in the G2/M phase. Comparedwith the control, the difference was significant in terms ofthe percentage of cells in the G2/M phase (P＜0.05). Allicincould inhibit telomerase activity in a time-dependent anddose-dependent pattern. After exposure to allicin at 0.016mg/ml for 24 hours, SGC-7901 cells showed typicalmorphologic change.CONCLUSION: Allicin can inhibit telomerase activity andinduce apoptosis of gastric cancer SGC-7901 cells. Allicinmay be more effective than AZT.
基金Supported by The Society Development Research Programs of Foundation Science and Technology Department of Jiangsu Province, No. BS99382the Science Basic Research Programs of University of Jiangsu Province, No. 06KJB360131
文摘AIM: To study the inhibitory effects of a Shuangling Fuzheng anticancer preparation (SFAP) on the human gastric cancer cell line SGC-7901 in vitro as well as its immune-modulated effects in a cyclophosphamide-treated murine model. METHODS: MTT experiments and immunocytochemistry ABC experiments were performed for detecting the proliferation of SGC-7901 cells in vitro and protein expression of c-myc. The staphylococcal protein A (SPA) rosette test was utilized for measuring the ratio of T-lymphocyte subsets from peripheral blood in a cyclophosphamide-treated murine model. Enzyme- linked immunosorbant assay (ELISA) was performed for measuring the levels of serum sIL-2R in treated mice, while immunoturbidimetry was used for measuring the levels of immunoglobulins (Ig). RESULTS: SFAP (40-640 mg/L, 48 h) inhibited the proliferation of SGC-7901 cells, and a positive correlation was noted between inhibitory effects and dosage. At a dosage of 160-320 mg/L in cultured cells, the expression of c-myc was decreased. SFAP (50-200 mg/kg) increased the percentage of CD3+ and CD4+ T-lymphocytes, the ratio of CD4/CD8, and the contents of Ig such as IgM, IgG or IgA, but decreased the levels of serum sIL-2R in peripheral blood from cyclophosphamide-treated mice. CONCLUSION: SFAP can inhibit the proliferation of SGC-7901 cells via the c-myc gene. In addition, SFAP can modulat the cellular and humoral immunity in cyclophosphamide-induced immunosuppressed mice.
基金National Natural Science Foundation of China,No.39870662
文摘AIM：Toinvestigate the effects of vitamin E succinate(VES)on the expression of c-jun gene and protein in human gastric cancer SGC-7901 cells.METHODS:After SGC-7901cells were treated with VESat different doses(5,10,20mg·L^-1)at different time,reverse transcription-PCR technique was used to detect the level of c-jun mRNA;Western Blot was applied to measure the expression of c-jun protein.RESULTS:After the cells were theated with VESat 20mg·L^-1for 3h,the expression rapidly reached its maximun that was3.5times of UT control(P<0.01).The level of c-jun mRNA was also increased following treatment of VESfor 6h.However the expression after treatment of VES at 5mg·L^-1for24h was 1.6tmes compared with UTcontrol(P<0.01),Western blot analysis showed that the level of c-jun protein was obviusly elevated in VES-treated SGC-7901cells at 20mg·L^-1for3h,The expression of c-jun protein was gradually increased after treatment of VES at 20mg·L^-1for3,6,12and24h,respectively,with an evident time-effect relationship.CONCONCLUSION:The levels of c-jun mRNA and protein in VES-treated SGC-7901cells were increased in a dose-and time-dependent manner;the expression of c-jun was prolonged by VES,indicating that c-jun is involvedin VES-induced apoptosis in SGC-7901 cells.
文摘AIM: To investigate the effects of mitomycin (MMC)combined with sulindac on cell viability, apoptotic induction and expression of apoptosis-related gene Bcl-2 and cyclooxygenase-2 (COX-2)in gastric cancer SGC-7901cells.METHODS: Human gastric cancer SGC-7901 cells were divided into three treatment groups,namely sulindac treatment group, MMC treatment group and combined sulindac with MMC treatment group. After being treated with drugs, cell viability was examined by MTr assay.Flow cytometry was used to evaluate the cell cycle distribution and apoptotic rates. Morphology of the cells was observed under light microscope and interactive laser microscope. Expression of COX-2 and Bcl-2 was determined by immunocytochemical method.RESULTS: After exposure for 12 h to three kinds of drugs,gastric cancer SGC-7901 cells presented some morphological features of apoptosis, including cell shrinkage, nuclear condensation, DNA fragmentation and formation of apoptotic bodies. Growth inhibition was more obvious in combined sulindac with MMC treatment group and sulindac treatment group than in MMC treatment group. The apoptotic rates in co-treated cells and MMC-treated cells 24 h after treatment were 12.0% and 7.2%, respectively.After exposure for 24 h to MMC, the expression of COX-2and Bcl-2 protein was up-regulated, COX-2 levels were down-regulated but Bcl-2 gene expression was not changed significantly in combined treatment group.CONCLUSION: MMC-induced apoptosis is reduced by up-regulating the expression of COX-2 and Bcl-2 genes.MMC combined with sulindac can suppress the growth of gastric cancer cells through induction of apoptosis mediated by down-regulation of apoptosis-related Bcl-2and COX-2 gene.
文摘AIM: To study the moleucle action mechunisms of NM-3 on the growth of human gastric cancer SGC-7901 cells in vivo or in vitro.METHODS: SGC-7901 from human non-differentiated gastric cancer cell line was cultured with NM-3 at 100 mg/ml for 24 h. We observed its inhibitory rate and the density of micro-vascular growth in grafted mice with human gastric cancer SGC-7901. The apoptosis of human gastric cancer SGC-7901 was revealed in NM-3 treatment group by using terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-fluorescene nick end labeling (TUNEL)method and flow cytometry analysis.RESULTS: The growth of SGC-7901 cells was markedly inhibited compared with control growp, which was smaller than that in normal saline control group (4.17 g±0.22 g VS 9.45 g±1.38 g, P＜0.01). The level of apoptosis of human gastric cell line SGC-7901 was obviously increased in NM-3treatment group at 1 mg.L-1 for 24 h. NM-3 inducing apoptotic index in NM-3 plus carboplatin group was 3.5 times that of carboplatin control group (TUNEL: 27.98±6.12 % VS 12.94±2.12 %, FACScan: 26.86±5.69 % VS11.86±1.09 %,P＜0.01). Western blot analysis showed that the apoptotic index of human gastric cancer was elevated for 12, 24 and 36 h with an evident time-effect relationship in groups at 100 mg.L-L. NM-3 enhanced the inhibitive effects and sensitivity of chemotherapy for human gastric cancer in nude mice. These results suggested that NM-3 played a key inhibitive role in the growth of grafted human gastric cancer in nude mice.CONCLUSION: NM-3 can inhibit the growth of human gastric cancer cell line SGC-7901, and enhance the sensitivity of carboplatin on SGC-7901 and induced its apoptosis.
基金Supported by Natural Science Research Project of Guangxi University of Chinese Medicine in 2015"Study on Anti-tumor Effect of Phyllanthus reticulatus Leaf Extract"(p15028)Independent Research Program of Guangxi Key Laboratory of Traditional Chinese Medicine Pharmacology in 2015"Study on Phyllanthus reticulatus Leaf 7404 Nude Mice Xenografts"+1 种基金Young Teachers Enhancement Project of Guangxi Department of Education in 2018"Study on the Mechanism of Zhuang Medicine Phyllanthus reticulatus Leaf against Liver Cancer"(2018KY0300)2019-2021 Guangxi First-class Discipline Construction Open Project Fund for Young Scholars of Guangxi University of Chinese Medicine"Anti-hepatocarcinoma Mechanism of Autophagy Induced by Ethyl Acetate in Phyllanthus reticulatus Leaf Based on PI3K/AKT and STAT3/m TOR Signaling Pathway"(2019XK089)
文摘[Objectives]To observe the effect of drug-containing serum from different extracts of Phyllanthus reticulatus leaf on the proliferation of human gastric cancer SGC-7901 cells and the effect of in vivo on the life extension rate of mice with H22 ascites tumor,and to investigate the effects of chemical components such as Corilagin,ethyl gallate,ethyl brevifolincarboxylate,and gallic acid on the proliferation of human gastric cancer SGC-7901 cells.[Methods]MTT method was used to observe the inhibitory effect of drug-containing serum of different extracts of P.reticulatus leaf on human gastric cancer SGC-7901 cells in vitro to determine its active site.The active site was used as the research object to establish a Kunming mouse ascites tumor model,to investigate the effect on the life extension rate of mice with H22 ascites tumor,to further separate the monomer components from the effective fraction and investigate its effect on human gastric cancer SGC-7901 cells.[Results]Compared with the 10%blank serum control group,10%drug-containing serum of ethyl acetate and n-butanol in P.reticulatus leaf had significant inhibitory effect on the proliferation of human gastric cancer SGC-7901 cells,and the inhibition rate was 34.99%and 28.68%,respectively(P<0.05).Compared with the blank group,the survival time of the high dose group of ethyl acetate in P.reticulatus leaf was significant(P<0.05).Gallic acid,Corilagin,and Brevifolincarboxylic acid ethyl ester had a significant inhibitory effect on the proliferation of human gastric cancer SGC-7901 cells,with IC 50 of 26.52,70.45,and 158.86μg/mL,respectively.Ethyl gallate had no inhibitory effect on the proliferation of human gastric cancer SGC-7901 cells,and its IC 50 was 251.96μg/mL.[Conclusions]The drug-containing serum of ethyl acetate and n-butanol extract of P.reticulatus can inhibit the proliferation of human gastric cancer SGC-7901 cells.Ethyl acetate of P.reticulatus leaves can increase the life extension rate of mice with H22 ascites tumor.Gallic acid,Corilagin,and Brevifolincarboxylic acid ethyl ester isolated from its active site are the material basis for inhibiting the proliferation of human gastric cancer SGC-7901 cells.
基金supported by the National Natural Science Foundation of China(NO.81760628).
文摘Objective: To investigate the cytotoxic effects and the potential mechanisms of crebanine N-oxide in SGC-7901 gastric adenocarcinoma cells. Methods: The cytotoxicity of crebanine N-oxide was evaluated by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay and cellular morphology was observed under a microscope. Cell apoptosis was determined by flow cytometry using propidium iodide staining. The expression levels of apoptotic-related proteins, cleaved caspase-3, cytochrome C, p53 and Bax, and autophagyrelated proteins p62, beclin1 and LC3 were detected by Western blotting assays. Results: Crebanine N-oxide treatment significantly inhibited the proliferation of SGC-7901 cells in a dose-dependent and timedependent manner via induction of G2-phase cell cycle arrest, apoptosis, and autophagy in SGC-7901 cells.Conclusions: Crebanine N-oxide could inhibit the growth of gastric cancer cells by promoting apoptosis and autophagy and could be used as a potential agent for treating gastric cancer.
基金supported by Harbin University of Commerce Research Funding(17x072)
文摘Objective： To investigate the effects of xanthotoxin from Apiaceae medicinal plants on cell proliferation and apoptosis, and explore its mechanism of action against human gastric carcinoma SGC-7901 cells in vitro.Methods： SGC-7901, HepG-2, MCF-7, and A549 cells were treated with different concentrations of xanthotoxin（10, 20, 60, 80, 100, 120, 140, and 160 μg/mL） for 48 h, and the cell viability（IC50） was determined by MTT assay; Xanthotoxin-induced apoptosis in cells was observed by using Hoechst 33258 Staining Kit and Annexin V-FITC Apoptosis Detection Kit; Flow cytometry was used to detect apoptosis related proteins of Fas/FasL, Bid, and DR5/TRAIL proteins in human gastric carcinoma SGC-7901 cells after being treated by xanthotoxin; The influence of xanthotoxin on Caspase-8 protein expression in the cells was determined by Flouormetric Assay Kit.Results： Xanthotoxin obviously inhibited SGC-7901, HepG-2, MCF-7, and A549 cells proliferation, and its inhibition was in a concentration-dependent manner; flow cytometry results showed that in a certain concentration range, xanthotoxin can increase the expression levels of Fas/FasL and DR5/TRAIL proteins in a concentration-dependence manner. The content of Bid protein in cells was increased, and it showed concentration-dependence.Conclusion： Xanthotoxin may induce SGC-7901 cells apoptosis in a certain concentration range through the Fas/FasL protein mediated death receptor pathway, or by DR5/TRAIL mediated death receptor pathway, and increase the expression level of death receptor protein, activation Caspase-8, activating downstream effect factor, inducing cell apoptosis, or activate Caspase-8 cutting activate protein Bid, and then enter the mitochondrial pathway, induction of apoptosis.
文摘AIM:To investigate the inhibitory effect of acetylshikonin on human gastric carcinoma cell line SGC-7901 and its mechanism. METHODS:MTT assay was used to assess the inhibitory effect of acetylshikonin on proliferation of SGC-7901 cells.Apopt osis-inducing effect was determined by flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling with Hoechst staining.Expression of mRNA and protein in Bcl-2 and Bax was analyzed by reverse transcription-polymerase chain reaction and Western blot.Antitumor effect of acetylshikonin on a mouse SGC-7901 model was also determined. RESULTS:Forty-eight hours after treatment with acetylshikonin,MTT assay showed that acetylshikonin inhibited the proliferation of SGC-7901 cells in a dose-dependent manner.The half maximal inhibitory concentration of acetylshikonin to SGC-7901 cells was 0.428±0.07 mg/L.Cell shrinkage,nuclear pyknosis and chromatin condensation,which are the characteristics of cell apoptosis,were observed in treated SGC-7901 cells and the percentage of apoptosis increased in a dose-dependent manner.Acetylshikonin downregulated the expression of Bcl-2 and up-regulated the expression of Bax in the treated SGC-7901 cells compared with the controls.The experiment in vivo showed that 0.5,1,and 2 mg/kg of acetylshikonin significantly inhibited the growth of tumor in the mouse SGC-7901 model,with an inhibitory rate of 25.00%-55.76%. CONCLUSION:Acetylshikonin inhibits the growth of SGC-7901 cells in vitro and in vivo by inducing cell apoptosis.
基金National Natural Science Foundation of China,No.39870662
文摘AIM:To investigate the effects of growth inhibition ofhuman gastric cancer SGC-7901 cell with RRR-α-tocopherylsuccinate(VES),a derivative of natural Vitamin E,viainducing apoptosis and DNA synthesis arrest.METHODS:Human gastric cancer SGC-7901 cells wereregularly incubated in the presence of VES at 5,10 and20mg.L^(-1)(VES was dissolved in absolute ethanol anddiluted in RPMI 1640 complete condition mediacorrespondingly to a final concentration of VES and lmL.L^(-1)ethanol),succinic acid and ethanol equivalents asvehicle(VEH)control and condition-media only asuntreated(UT)control.Trypan blue dye exclusionanalysis and MTT assay were applied to detect the cellproliferation.37kBq of tritiated thymidine was added tocells and [~3H]TdR uptake was measured to observe DNAsynthesis.Apoptotic morphology was observed byelectron microscopy and DAPI staining.Flow cytometryand terminal deoxynucleotidyl transferase-mediated dUTPnick end labeling(TUNEL)assay were performed to detectVES-triggered apoptosis.RESULTS:VES inhibited SGC-7901 cell growth in a dose-dependent manner.The growth curve showed suppressionby 24.7%,49.2% and 68.7% following 24h of VEStreatment at 5,10 and 20 mg·L^(-1),respectively,similar tothe findings from MTT assay.DNA synthesis wasevidently reduced by 35%,45% and 98% after 24h VEStreatment at 20 mg·L^(-1)and 48h at 10 and 20 mg·L^(-1),respectively.VES induced SGC-7901 cells to undergoapoptosis with typically apoptotic characteristics,including morphological changes of.chromatincondensation,chromatincrescent formation/margination,nucleus fragmentation and apoptotic body formation,typical apoptotic sub-G1 peak by flow cytometry andincrease of apoptotic cells by TUNEL assay in which 90%of cells underwent apoptosis after 48h of VES treatment at20 mg·L^(-1).CONCLUSION:VES can inhibit human gastric cancer SGC-7901 cell growth by inducing apoptosis and DNA synthesisarrest,inhibition of SGC-7901 cell growth by VES is dose-and time-dependent.Therefore VES can function as apotent chemotherapeutic agent against human gastric carcinogenesis.
基金the National Natural Science Foundation of China,No.39870661
文摘AIM: To determine the effect of apoptosis on gastric cancer cells (SGC-7901) induced by cis-9, trans-11-conjugated linoleic acid (c9, t11-CLA) and its possible mechanism in the inhibition of cancer cells growth.METHODS: Using cell culture, flow cytometery and immunocytochemical techniques, we examined the cell growth, frequency of apoptosis and distribution of cell cycle,expression of ki67, bcl-2, Fas, and c-myc of SGC-7901 cells which were treated with various c9, t11-CLA concentrations (25,50,100 and 200 μmol@L-1) of c9, t11-CLA for 24h and 48 h,with a negative control (0.1% ethanol).RESULTS: The growth of SGC-7901 cells was inhibited by c9,t11-CLA. Eight days after treatment with various concentrations of c9,t11-CLA, as mentioned above, the inhibition rates were 5.9 %, 20.2 %,75.6 % and 82.4 %, respectively. The frequency of apoptosis on SGC-7901 cells induced by different concentrations of c9, t11-CLA (except for 25 μmol@L-1, 24 h) was significantly greater than that in the negative control (P＜0.01). To further investigate the influence of the cell cycle progression, we found that apoptosis induced by c9, t11-CLA may be involved in blocking the cell cycle of SGC-7901 cells. Immunocytochemical staining demonstrated that SGC-7901 cells preincubated in media supplemented with different c9, t11-CLA concentrations for various time periods significantly decreased the expressions of ki67 (the expression rates were 18.70-3.20 %, at 24 h and 8.10-0.20 % at 48 h, respectively), bd-2 (4.30-0.15 % at 24 h and 8.05 %-0 at 48 h),and c-myc(4.85-2.20 % at 24 h and 4.75-0.30 % at 48 h) as compared with those in the controls (the expressions of ki67, bcl-2, and c-mycwere 15.1% at 24 h and 13.5 % at 48 h, 6.80 % at 24 h and 8.00 % at 48 h,5.50 % at 24 h and 5.30 % at 48 h, respectively) (P＜0.01),whereas the expressions of Fas were increased (0.60-2.75 %,24 h and 0.45-5.95 %, 48 h).CONCLUSION: The growth and proliferation of SGC-7901 cells are inhibited by cg, t11-CLA via blocking the cell cycle,pathways of bcl-2-associated mitochondria with reduced expression of bcl-2 and Fas-associated death domain protein (FADD) with enhanced expression of Fas. But expression of c-myc on SGC-7901 cells is lower than that in negative control, which needs to be studied further.
基金the National Natural Science Foundation of China, No.30070658
文摘AIM: To investigate the effect of c9, t1l-conjugated linoleic acid (c9, t11-CLA) on the invasion of human gastric carcinoma cell line and its possible mechanism of preventing metastasis.METHODS: Using reconstituted basement membrane invasion, chemotaxis, adhesion, PAGE substrate zymography and RT-PCR assays, we analyzed the abilities of invasion,direct migration, adhesion of intracellular matrix, as well as the activity of type IV collagenase and expression of tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 mRNA in SGC-7901 cells which were treated with gradually increased concentrations (25, 50, 100 and 200μmol/L) of c9,c11-CLA for 24 h.RESULTS: At the concentrations of 200μmol/L, 100μmol/L and 50μmol/L, c9,tll-CLA suppressed the invasion of SGC-7901 cells into the reconstituted basement membrane by 53.7 %, 40.9 % and 29.3 %, respectively, in comparison with the negative control. Only in the 200 μmol/L c9,tll-CLA group, the chemotaxis of SGC-7901 cells was inhibited by 16.0 % in comparision with the negative control. C9,tll-CLA also could inhibit the adhesion of SGC-7901 cells to laminin, fibronectin and Matrigel, increase the expression of TIMP-1 and TIMP-2 mRNA, and reduce type IV collegenase activities in the serum-free medium supernatant of SGC-7901 cells.CONCLUSION: c9,t11-C:LA can inhibit the invasion of SGC-7901 cells at multiple procedures in tumor metastasis cascade, which may be associated with the induction of TIMP-1 and TIMP-2 mRNA expression.
基金the Major State Basic Research(973)Program of China,(G1999053905)National Natural Science Foundation of China,No.30170207
文摘AIM: To evaluate the effects of tributyrin, a pro-drug of natural butyrate and a neutral short-chain fatty acid triglyceride, on the growth inhibition of human gastric cancer SGC-7901 cell.METHODS: Human gastric cancer SGC-7901 cells were exposed to tributyrin at 0.5, 1, 2, 5, 10 and 50 mmol·L-^1 for 24-72h. MTT assay was applied to detect the cell proliferation.[^3H]-TdR uptake was measured to determine DNA synthesis.Apoptotic morphology was observed by electron microscopy and Hoechst-33258 staining. Flow cytometry and terminal deoxynudeotidyl transferase-mediated dUTP nick end labeling(TUNEL) assay were performed to detect tributyrin-triggered apoptosis. The expressions of PARP, Bcl-2 and Bax were examined by Western blot assay.RESULTS: Tributyrin could initiate growth inhibition of SGC-7901 cell in a dose-and time-dependent manner. [^3H]-TdR uptake by SGC-7901 cells was reduced to 33.6% after 48h treatment with 2mmol·L^-1 tributyrin, compared with the control (P<0.05). Apoptotic morphology was dell:ted by TUNEL assay. Flow cytometry revealed that tributyrin could induce apoptosis of SGC-7901 cells in dose-dependent manner. After 48 hours incubation with tributyrin at 2mmol·L^-1, the level of Bcl-2 protein was lowered, and the level of Bax protein was increased in SGC-7901, accompanied by PARP cleavage.CONCLUSION: Tributyrin could inhibit the growth of gastric cancer cells effectively in vitro by inhibiting DNA synthesis and inducing apoptosis, which was associated with the downregulated Bcl-2 expression and the up-regulated Bax expression. Therefore, tribublrin might be a promising chemopreventive and chemotherapeutic agent against human gastric carcinogenesis.
基金Supported by the National Key Research Project Foundation of China,No.96-905-02-01,and the National Natural Science Foundation of China,No.39630340
文摘AIM: To explore the effects of mifepristone, a progesterone receptor (PR) antagonist, on the proliferation of human gastric adenocarcinoma cell line SGC-7 901 in vitro and the possible mechanisms involved.METHODS: In situ hybridization was used to detect the expression of PR mRNA in SGC-7 901 cells. After treatment with various concentrations of mifepristone (2.5, 5, 10,20μmol/L) at various time intervals, the ultrastructural changes, cell proliferation, cell-cycle phase distribution, and the expression of caspase-3 and Bcl-XL were analyzed using transmission electron microscopy (TEM), tetrazolium blue (MTT) assay, ^3H-TdR incorporation, flow cytometry, and reverse transcription-polymerase chain reaction (RT-PCR).RESULTS: Mifepristone markedly induced apoptosis and inhibited cell proliferation of PR- positive SGC-7 901 cells revealed by TEM, MTT assay and ^3H-TdR incorporation, in a dose- and time-dependent manner. The inhibitory rate was increased from 8.98% to 51.29%. Flow cytometric analysis showed mifepristone dose-dependently decreased cells in S and G2/M phases, increased cells in G0/G1 phase,reduced the proliferative index from 57.75% to 22.83%.In addition, mifepristone up-regulated the expression of caspase-3, and down- regulated the Bcl-XL expression,dose-dependently.CONCLUSION: Mifepristone effectively inhibited the proliferation of PR-positive human gastric adenocarcinoma cell line SGC-7 901 in vilrothrough multiple mechanisms, and may be a beneficial agent against human adenocarcinoma.
