KCNQ1OT1 通过调节 MIR-142-5p/CAPN10 轴促进卵巢癌细胞的进展。
KCNQ1OT1 promotes ovarian cancer progression via modulating MIR-142-5p/CAPN10 axis.
机构信息
Department of Gynecology, Women and Children's Hospital, School of Medicine, Xiamen University, Fujian, China.
出版信息
Mol Genet Genomic Med. 2020 Feb;8(2):e1077. doi: 10.1002/mgg3.1077. Epub 2020 Jan 7.
BACKGROUND
Long non-coding RNA (lncRNA) has been regarded as crucial regulator for cancer progression. Roles of KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) in cancers including osteosarcoma and colon cancer have been previously reported. However, its role in ovarian cancer (OC) remains unclear.
METHODS
Expression level of KCNQ1OT1 on OC cells and normal cell was analyzed with quantitative real-time PCR. Gain and loss-of-function experiments were performed to analyze the biological roles of KCNQ1OT1 in OC. Moreover, whether KCNQ1OT1 functions its role via mediating MICRORNA-142-5p (MIR-142-5p)/calpain 10 (CAPN10) axis was analyzed. In addition, effects of KCNQ1OT1, MIR-142-5p, and CAPN10 on overall survival of OC patients were analyzed at Kaplan-Meier plotter website.
RESULTS
We showed KCNQ1OT1 was elevated expression in OC cells and indicated poorer overall survival of OC patients. Besides, we found KCNQ1OT1 could promote OC cell proliferation and migration in vitro. Moreover, MIR-142-5p was found reduced expression, while CAPN10 was found elevated expression in OC cells compared with normal cell. Kaplan-Meier curve analysis showed low MIR-142-5p or high CAPN10 expression were indicators for poorer overall survival of OC patients. At length, we showed KCNQ1OT1 could regulate OC development via MIR-142-5p/CAPN10 axis.
CONCLUSIONS
Taken together, KCNQ1OT1 upregulates CAPN10 expression via sponging MIR-142-5p, thus promoting the proliferation and migration of OC.
背景
长链非编码 RNA（lncRNA）已被认为是癌症进展的关键调节因子。先前已经报道了 KCNQ1 反义转录本 1（KCNQ1OT1）在包括骨肉瘤和结肠癌在内的癌症中的作用。然而，其在卵巢癌（OC）中的作用尚不清楚。
方法
使用定量实时 PCR 分析 OC 细胞和正常细胞中 KCNQ1OT1 的表达水平。进行增益和失活功能实验，以分析 KCNQ1OT1 在 OC 中的生物学作用。此外，还分析了 KCNQ1OT1 是否通过调节微小 RNA-142-5p（MIR-142-5p）/钙蛋白酶 10（CAPN10）轴发挥其作用。此外，在 Kaplan-Meier plotter 网站上分析了 KCNQ1OT1、MIR-142-5p 和 CAPN10 对 OC 患者总生存期的影响。
结果
我们表明 KCNQ1OT1 在 OC 细胞中表达上调，并表明 OC 患者的总体生存率较差。此外，我们发现 KCNQ1OT1 可以促进 OC 细胞在体外的增殖和迁移。此外，与正常细胞相比，OC 细胞中 MIR-142-5p 的表达降低，而 CAPN10 的表达升高。Kaplan-Meier 曲线分析表明，MIR-142-5p 表达低或 CAPN10 表达高是 OC 患者总体生存率较差的指标。最后，我们表明 KCNQ1OT1 可以通过 MIR-142-5p/CAPN10 轴调节 OC 的发展。
结论
总之，KCNQ1OT1 通过海绵吸附 MIR-142-5p 上调 CAPN10 的表达，从而促进 OC 的增殖和迁移。
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