Objective Tumors with accelerated growth or high malignancy are thought to undergo active angio- genesis. Whereas by far, there is few study concerning the combination of MIB-1 proliferation index (MIB-1 PI) and tumor...Objective Tumors with accelerated growth or high malignancy are thought to undergo active angio- genesis. Whereas by far, there is few study concerning the combination of MIB-1 proliferation index (MIB-1 PI) and tumor angiogenesis in carcinomas to show their significance in relate to clinicopathological parameters. In the present study, we evaluated the significance or MIB-1 PI and angiogenesis in early stage of gastric cancer. Our focus was es- pecially on the combination of MIB-1 PI and angiogenesis in relate to lymph node metastasis. Method Specimens from 95 patients with early gastric cancer were studied by means or immunohistochemistry using monoclonal MIB-1 and factor Ⅷ related antigen antibodies. Results The mean MIB-1 PI and microvessel count were 22.9% and 34.7, respectively. The MIB-1 PI did not correlate with microvessel count. Both correlated with depth of tumor invasion, lymphatic vessel invasion and lymph node metastasis. Multivarlate analysis showed that combined high MIB-1 PI/hy- pervascularity, as well as lymphatic vessel invasion and tumor size were independent factors that impact on lymph node metastasis. Conclusion A combination of the high MIB-1 PI/hypervascularity is a factor that related to lymph node metastasis in early gastric cancer.展开更多
Objective: To investigate the effects and mechanisms of p38 signaling pathway in pentagastrin-regulated cell proliferation of colorectal carcinoma cell line HT-29. Methods: HT-29 cell line of colorectal carcinoma was ...Objective: To investigate the effects and mechanisms of p38 signaling pathway in pentagastrin-regulated cell proliferation of colorectal carcinoma cell line HT-29. Methods: HT-29 cell line of colorectal carcinoma was in vitro incubated and divided into the control group, pentagastrin group, proglumide group, and pentagastrin + proglumide group. MTT reduction assay was performed to detect the proliferation status of HT-29 cell line and determine the optimal dosage of pentagastrin and proglumide. Annexin V-fluorescein isothiocyanate flow cytometry was used to detect the proliferation index (PI) and apoptosis rate (AR) of HT-29 cells. Reverse transcriptase polymerase chain reaction was performed to detect the mRNA expression of the pentagastrin receptor/cholecystokinin-B receptor (CCK-BR) and p38. The protein and phosphorylation levels of p38 were estimated by western blotting. Results: RT-PCR detection showed that CCK-BR mRNA was expressed in the HT-29 cell line. Pentagatrin improved HT-29 cell proliferation in dosage of 6.25 - 100 mg/L, and the optimal dosage of pentagastrin was 25.0 mg/L. Proglumide had no significant effect on the proliferation of HT-29 cells, but significantly inhibited the proliferation of HT-29 cells stimulated by pentagastrin when the dosage of proglumide was 8.0 - 128.0 mg/L, and the optimal dosage was 32.0 mg/L. The AR in the pentagastrin group was significantly lower than that in the control group and in the pentagastrin + proglumide group. The PI in the pentagastrin group was significantly higher than that in the control group and in the pentagastrin + proglumide group. P38 phosphorylation level in the pentagastrin group was significantly lower than that in the control group, and in the pentagastrin + proglumide group. There were no significant differences in the mRNA and protein expression of p38 in the control, pentagastrin, proglumide and pentagastrin + proglumide groups. Conclusion: Pentagastrin can improve proliferation of the CRC cell line HT-29 and inhibit apoptosis via the p38 signal transduction pathway. This mechanism may be associated with suppressed p38 protein phosphorylation level due to inhibition of proglumide, a gastrin receptor antagonist.展开更多
文摘Objective Tumors with accelerated growth or high malignancy are thought to undergo active angio- genesis. Whereas by far, there is few study concerning the combination of MIB-1 proliferation index (MIB-1 PI) and tumor angiogenesis in carcinomas to show their significance in relate to clinicopathological parameters. In the present study, we evaluated the significance or MIB-1 PI and angiogenesis in early stage of gastric cancer. Our focus was es- pecially on the combination of MIB-1 PI and angiogenesis in relate to lymph node metastasis. Method Specimens from 95 patients with early gastric cancer were studied by means or immunohistochemistry using monoclonal MIB-1 and factor Ⅷ related antigen antibodies. Results The mean MIB-1 PI and microvessel count were 22.9% and 34.7, respectively. The MIB-1 PI did not correlate with microvessel count. Both correlated with depth of tumor invasion, lymphatic vessel invasion and lymph node metastasis. Multivarlate analysis showed that combined high MIB-1 PI/hy- pervascularity, as well as lymphatic vessel invasion and tumor size were independent factors that impact on lymph node metastasis. Conclusion A combination of the high MIB-1 PI/hypervascularity is a factor that related to lymph node metastasis in early gastric cancer.
文摘Objective: To investigate the effects and mechanisms of p38 signaling pathway in pentagastrin-regulated cell proliferation of colorectal carcinoma cell line HT-29. Methods: HT-29 cell line of colorectal carcinoma was in vitro incubated and divided into the control group, pentagastrin group, proglumide group, and pentagastrin + proglumide group. MTT reduction assay was performed to detect the proliferation status of HT-29 cell line and determine the optimal dosage of pentagastrin and proglumide. Annexin V-fluorescein isothiocyanate flow cytometry was used to detect the proliferation index (PI) and apoptosis rate (AR) of HT-29 cells. Reverse transcriptase polymerase chain reaction was performed to detect the mRNA expression of the pentagastrin receptor/cholecystokinin-B receptor (CCK-BR) and p38. The protein and phosphorylation levels of p38 were estimated by western blotting. Results: RT-PCR detection showed that CCK-BR mRNA was expressed in the HT-29 cell line. Pentagatrin improved HT-29 cell proliferation in dosage of 6.25 - 100 mg/L, and the optimal dosage of pentagastrin was 25.0 mg/L. Proglumide had no significant effect on the proliferation of HT-29 cells, but significantly inhibited the proliferation of HT-29 cells stimulated by pentagastrin when the dosage of proglumide was 8.0 - 128.0 mg/L, and the optimal dosage was 32.0 mg/L. The AR in the pentagastrin group was significantly lower than that in the control group and in the pentagastrin + proglumide group. The PI in the pentagastrin group was significantly higher than that in the control group and in the pentagastrin + proglumide group. P38 phosphorylation level in the pentagastrin group was significantly lower than that in the control group, and in the pentagastrin + proglumide group. There were no significant differences in the mRNA and protein expression of p38 in the control, pentagastrin, proglumide and pentagastrin + proglumide groups. Conclusion: Pentagastrin can improve proliferation of the CRC cell line HT-29 and inhibit apoptosis via the p38 signal transduction pathway. This mechanism may be associated with suppressed p38 protein phosphorylation level due to inhibition of proglumide, a gastrin receptor antagonist.
