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）
作者单位邮编
缪晓宇 大连理工大学 116024
肖桂山* 大连理工大学 116024
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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