过表达SARI通过抑制AP-1转录并下调抗凋亡分子Mcl-1的表达诱导宫颈癌细胞凋亡

发布时间：2019-06-20 01:30

【摘要】：目的探讨过表达SARI(suppressor of AP-1 and regulated by IFN)对宫颈癌细胞增殖的影响及可能的分子机制。方法在He La细胞和Ca Ski细胞转染可表达SARI的质粒后,使用Real-time PCR和Western blot检测细胞中SARI表达水平的变化;CCK-8法检测上述宫颈癌细胞模型的增殖;流式细胞术分析上述细胞模型的周期及凋亡;报告基因检测转录因子AP-1的转录活性;Western blot检测抗凋亡分子Mcl-1及Bcl-2的表达。结果成功构建过表达SARI的细胞模型。SARI表达水平上调后,细胞增殖受到抑制(P0.01);早期凋亡细胞增加但细胞周期无明显变化。转录因子AP-1的转录活性及Mcl-1的表达明显下调(P0.05),但Bcl-2的表达无明显变化。结论宫颈癌细胞中过表达SARI诱导宫颈癌细胞发生早期凋亡,可能是通过抑制AP-1的转录并下调抗凋亡分子Mcl-1的表达来实现的。
[Abstract]:Objective to investigate the effect of overexpression of SARI (suppressor of AP-1 and regulated by IFN) on the proliferation of cervical cancer cells and its possible molecular mechanism. Methods the expression of SARI in He La cells and Ca Ski cells was detected by Real-time PCR and Western blot, the proliferation of cervical cancer cell models was detected by CCK-8 assay, the cycle and apoptosis of the above cell models were analyzed by flow cytometry, and the expression of anti-apoptotic molecules Mcl-1 and Bcl-2 was detected by reporter gene detection of transcription factor AP-1 transcriptional activity; Western blot. Results the cell model of overexpression of SARI was successfully constructed. After the expression level of sari was up-regulated, the cell proliferation was inhibited (P01), and the early apoptotic cells increased but the cell cycle did not change significantly. The transcriptional activity of transcription factor AP-1 and the expression of Mcl-1 were significantly down-regulated (P 0.05), but the expression of Bcl-2 had no significant change. Conclusion overexpression of SARI in cervical cancer cells can induce early apoptosis of cervical cancer cells, which may be achieved by inhibiting the transcription of AP-1 and down-regulating the expression of anti-apoptotic molecule Mcl-1.
【作者单位】：第三军医大学基础医学部生物化学与分子生物学教研室;第三军医大学大坪医院野战外科研究所妇产科;
【基金】：国家自然科学基金面上项目(81272865);国家自然科学基金青年科学基金(81402268) 重庆市自科学基金(CSTC2013jj B10015)~~
【分类号】：R737.33

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