文章摘要
OLA1通过抑制细胞凋亡影响乳腺癌细胞耐药性的机制探讨
Mechanism of OLA1 affecting drug resistance of breast cancer cells by inhibiting apoptosis
投稿时间:2019-03-12  修订日期:2019-04-02
DOI:
中文关键词: 乳腺癌  耐药性  OLA1  细胞凋亡  机制
英文关键词: breast cancer  drug resistance  OLA1  apoptosis  mechanism
基金项目:国家自然科学基金项目(面上项目,重点项目,重大项目)
作者单位E-mail
缪晓宇 大连理工大学 mxy123@mail.dlut.edu.cn 
肖桂山 大连理工大学 gxiao@dlut.edu.cn 
刘建洲 大连理工大学  
杨青 大连理工大学  
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中文摘要:
      目的:研究OLA1表达变化对紫杉醇作用于乳腺癌细胞MCF-7的影响及具体机制。方法:使用检索工具GEPIA检索OLA1在人体内表达情况。通过低浓度梯度诱导法构建乳腺癌细胞MCF-7关于紫杉醇的耐药细胞株,用MTT法检验细胞耐药性,利用Western Blot检测目标蛋白在细胞内的表达变化。依靠siRNA转染降低耐药细胞株内OLA1表达。使用流式细胞仪检测OLA1变化对细胞凋亡影响。结果:OLA1在人体内广泛存在,并且在肿瘤组织与正常组织间有差异表达。MCF-7对紫杉醇的耐药性经过诱导,耐药指数达到15.2。OLA1表达水平随着细胞耐药性增加而提高(P<0.01),当敲低耐药株中OLA1表达水平,耐药性随之减少,同时,抗凋亡蛋白BCL-2表达升高,促凋亡蛋白Bax、Caspase-3表达升高,细胞凋亡率也随之增加。结论:OLA1通过影响细胞凋亡相关蛋白表达,降低紫杉醇对乳腺癌细胞的杀伤效果,由此提高乳腺癌细胞对药物的耐受性。
英文摘要:
      Objective: To investigate the effect of OLA1 on the drug resistance of breast cancer cells MCF-7 and its specific mechanism Methods: The bioinformatics website GEPIA was applied to search for the expression of OLA1 in humans. The drug-resistant cell line MCF-7 related to paclitaxel was constructed by low concentra-tion gradient induction method. The drug resistance was tested by MTT, and the ex-pression of target protein in the cells was detected by Western Blot. The expression of OLA1 in drug-resistant cell lines was reduced by siRNA transfection .Flow cytometry was used to study the effect of OLA1 changes on apoptosis. Results: OLA1 is widely expressed in humans and has different expression between tumor tissues and normal tissues. The resistance of MCF-7 to paclitaxel was induced and its drug re-sistance index reached 15.2. The expression of OLA1 increased with the increase of cell drug resistance (P<0.01). When knocking down OLA1 in drug-resistant cells, the drug resistance decreased and the expression of anti-apoptotic protein BCL-2 in-creased. The expression of Pro-apoptosis protein Bax and Caspase-3 increased. At the same time, the rate of cell apoptosis increased. Conclusion: OLA1 enhances the tolerance of breast cancer cells to paclitaxel by affecting apoptosis-related proteins.
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