Abstract
BackgroundLong 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.MethodsExpression 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.ResultsWe 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.ConclusionsTaken together, KCNQ1OT1 upregulates CAPN10 expression via sponging MIR‐142‐5p, thus promoting the proliferation and migration of OC.
Highlights
Ovarian cancer (OC) is a common occurred cancer type in female reproductive system (Siegel, Miller, & Jemal, 2018).The 5-year overall survival for ovarian cancer (OC) patients is about 30% due to approximately 75% of cancer patients are diagnosed at late stages (Siegel, Miller, & Jemal, 2017; Sorensen, Schnack, Karlsen, & Hogdall, 2015)
A recent work conducted by Zhao et al revealed several Long non-coding RNA (lncRNA)/miRNA/mRNA triplets that may contribute to the cisplatin-resistant in epithelial OC (Zhao, Tang, Zuo, Zhang, & Wang, 2019)
Previous studies have suggested that lncRNA KCNQ1OT1 plays crucial roles in cancer biology (Li et al, 2019; Xian & Zhao, 2019)
Summary
Ovarian cancer (OC) is a common occurred cancer type in female reproductive system (Siegel, Miller, & Jemal, 2018). The overexpression of FLVCR1-AS1 was revealed to promote cancer proliferation, metastasis, and epithelial to mesenchymal transition via regulating Yes associated protein 1 (606608) expression via modulating MICRORNA-513, while the knockdown of FLVCR1-AS1 caused opposite effects on OC cell behaviors (Yan et al, 2019). KCNQ1OT1 was identified to be elevated expression and correlated with poor overall survival of cancer patients (Li et al, 2019). It was found knockdown of KCNQ1OT1 inhibits cell proliferation but promotes cell apoptosis through MIR-34a (611172)/ autophagy-related 4B cysteine peptidase (611338) (Li et al, 2019). The underlying mechanism of KCNQ1OT1 in regulating OC cell behaviors was explored
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