LINC00536靶向miR-17-5p对卵巢癌细胞顺铂药物耐药性的影响  

The Effect of LINC00536 on Cisplatin Resistance of Ovarian Cancer Cells by Targeting MiR-17-5p

作　　者：赵营 赵光日 吴蕴瑜 吕晓刚 ZHAO Ying;ZHAO Guangri;WU Yunyu;LYU Xiaogang(Department of Gynecologic Oncology Surgery, Affiliated Tumor Hospital of Guangzhou Medical University,Guangzhou 510095, China)

机构地区：[1]广州医科大学附属肿瘤医院妇科肿瘤外科,广东广州510095

出　　处：《标记免疫分析与临床》2020年第11期1964-1969,共6页Labeled Immunoassays and Clinical Medicine

摘　　要：目的研究LINC00536对卵巢癌细胞增殖、凋亡和顺铂(DDP)敏感性的影响及潜在作用机制。方法qRT-PCR检测卵巢癌组织和卵巢癌细胞系COC1和COC1/DDP中LINC00536的水平,然后在COC1/DDP细胞中转染si-LINC00536和/或anti-miR-17-5p表达,用2.5μg/mL DDP处理COC1/DDP细胞,MTT法和流式细胞术测定COC1/DDP细胞存活率、凋亡率和细胞周期;Western blot检测细胞中Ki67和clv-caspase-3蛋白表达,双荧光素酶报告系统验证LINC00536和miR-17-5p的靶向关系。结果与癌旁组织相比,卵巢癌组织中LINC00536的水平显著上调(P<0.05);与卵巢癌细胞COC1相比,耐顺铂细胞COC1/DDP中LINC00536的水平也显著上调(P<0.05);2.5μg/mL DDP处理COC1/DDP细胞后,COC1/DDP细胞G0期细胞百分比升高,S期细胞百分比降低,细胞存活率显著降低,细胞凋亡率升高;抑制LINC00536可提高COC1/DDP细胞凋亡率、clv-caspase-3蛋白表达量和G0期细胞百分比;降低COC1/DDP细胞存活率、Ki67蛋白水平及S期细胞百分比;LINC00536靶向负调控miR-17-5p的表达;抑制miR-17-5p能逆转抑制LINC00536对DDP处理的COC1/DDP增殖、凋亡的作用。结论LINC00536可靶向miR-17-5p调控卵巢癌COC1/DDP细胞增殖、凋亡及其对顺铂的敏感性。LINC00536有望成为卵巢癌顺铂增敏靶点。Objective To investigate the effect of LINC00536 on proliferation,apoptosis and cisplatin sensitivity of ovarian cancer cells and its potential mechanism.Methods The levels of LINC00536 in ovarian cancer tissues and cell lines COC1 and COC1/DDP were detected by qRT-PCR,and then the si-LINC00536 and/or anti-miR-17-5p was transfected in COC1/DDP cells.COC1/DDP cells were treated with 2.5μg/ml DDP,then the survival rate,apoptosis rate and cell cycle of COC1/DDP cells treated with DDP were measured by MTT assay and flow cytometry.The expression levels of Ki67 and clv-caspase-3 proteins were detected by western blot,and the targeting relationship between LiNC00536 and miR-17-5p was verified by a dual-luciferase report system.Results Compared with the adjacent tissue group,the level of LINC00536 in the ovarian cancer tissue group was significantly increased(P<0.05).Compared with ovarian cancer cell COC1,the level of LINC00536 in cisplatin-resistant cell COC1/DDP was also remarkably increased(P<0.05).After 2.5μg/mL DDP treatment of COC1/DDP cells,the percentage of cells in G0 phase was increased,while the percentage of cells in S phase was decreased,and the cell survival rate was significantly decreased,while the cell apoptosis rate was increased.Inhibition of LINC00536 increased the apoptosis rate of COC1/DDP cells treated with DDP,the expression level of clv-caspase-3 protein and the percentage of G0 cells,while the survival rate,Ki67 protein content and S phase cell percentage of COC1/DDP cells were all reduced.LINC00536 negatively regulated the expression of miR-17-5p.Inhibition of miR-17-5p reversed the effect of LINC00536 inhibition on proliferation and apoptosis of COC1/DDP cells treated by DDP.Conclusion LINC00536 regulates the proliferation,apoptosis and cisplatin sensitivity of ovarian cancer COC1/DDP cells by targeting miR-17-5p.In light of that,LINC00536 is expected to be a cisplatin sensitization target for ovarian cancer.

关 键 词：卵巢癌 COC1/DDP LINC00536 miR-17-5p 顺铂敏感性 增殖 凋亡 

分 类 号：R737.31[医药卫生—肿瘤]