摘要
目的:探讨125IUdR偶联c-myb反义寡核苷酸对C6脑胶质瘤细胞增殖和凋亡的影响及可能的机制。方法:60只大鼠随机余数法分成对照组、c-myb-ASODN处理组和125IUdR-ASODN处理组。MTT和TUNEL法检测各组大鼠肿瘤细胞增殖抑制率和凋亡率;免疫组化法检测Bax和Bcl-xl蛋白表达;RT-PCR法检测BaxmRNA和Bcl-xlmRNA含量;Western-blot法检测c-myb蛋白表达。结果:125IUdR-ASODN处理组C6胶质瘤细胞的增殖抑制率和细胞凋亡率(69·81%和11·03%)增高均较c-myb-ASODN处理组(40·37%和6·48%)增高,P均<0·01;与对照组凋亡率(0·95%)比较,差异有统计学意义,P均<0·01。c-myb-ASODN处理组和125IUdR-ASODN处理组C6胶质瘤细胞的Bax蛋白194·6±6·25增高及Bcl-xl蛋白59·0±3·56下降较ASODN组Bax蛋白147·4±5·23增高及Bcl-xl蛋白83·9±3·93下降,P均<0·01;125IUdR-ASODN和ASODN处理组BaxmRNA表达随着时间延长而显著升高,Bcl-xlmRNA及c-myb蛋白表达随着时间延长而显著下降,P均<0·01;且125IUdR-ASODN的作用明显强于c-myb-ASODN,P<0·01。结论:c-myb-ASODN和125IUdR-ASODN均具有促进C6胶质瘤细胞凋亡和抑制其增殖的作用,且125IUdR-ASODN的作用更为显著;c-myb-ASODN和125IUdR-ASODN可能通过Bax/Bcl-xl途径诱导C6胶质瘤细胞凋亡,其对Bax和Bcl-xl的调节发生在转录水平前的某一环节。
OBJECTIVE： To explore the proliferation and apoptosis of C6 glioma cells administrated by ^125IUdR-ASODN and their possible mechanism. METHODS.. C6 glioma cells were implanted into the abdominal cavities of the sixty rats to establish experimental models. There were control, ASODN and ^125IUdR-ASODN groups. Cell growth inhibitory rate, apoptosis rate and Bax, Bcl-xl protein expression were determined; By MTT, TUNEL and immunohistochemical technique, RT-PCR was applied to check BaxmRNA and BclxlmRNA; Western-blot was performed to detected c-myb protein expression. RESULTS： The cell growth inhibitory rate, apoptosis rate of ^125 IUdR-ASODN group （69.81% and 11.03%） were higher than those of ASODN group（40.37% and 6. 48%） ,P〈0.01; compared with that of control group （apoptosis rate is 0.95 % ）, there were statistically significant difference, P 〈 0. 01. Bax protein, Bax mRNA ascend and Bcl-xl protein, Bcl-xl mRNA, c-myb protein descend along with the time prolonged of ASODN and ^125IUdR-ASODN, and there were statistically significant difference between the different groups, P〈0.01 ; and the effect of ^125IUdR-ASODN group were all more obvious than those of ASODN group, P〈0.01. CONCLUSIONS： ASODN and ^125IUdR-ASODN have the function of antiproliferation and inducing apoptosis on C6 cells. The function of ^125IUdR-ASODN is more apparent than that of ASODN; It is a posssble Asodn and ^125IUdR-ASODN inducing apoptosis on C6 cells by a regulation pathway of Bax/Bclxl. The regulation of Bax and Bcl-xl by ASODN and ^125IUdR-ASODN occurs at a point before transduction,
出处
《中华肿瘤防治杂志》
CAS
2006年第6期414-418,共5页
Chinese Journal of Cancer Prevention and Treatment
