Abstract
BackgroundThe large involvement of long non-coding RNAs (LncRNAs) in the biological progression of numerous cancers has been reported. The function of lncRNA KCNQ1OT1 in bladder cancer (BC) remains largely unknown. This study aimed to explore the critical role of KCNQ1OT1 in BC.Materials and methodsThe qRT-PCR was applied to test the expression of RNAs. Cell proliferation was detected by CCK-8 and colony formation assays. Cell apoptosis was measured by TUNEL and flow cytometry experiments. Wound healing and transwell assays were employed to evaluate cell migration and invasion ability respectively. Western blot assay was used to measure relevant protein expression. Immunofluorescence (IF) staining was used to observe EMT process in BC.ResultsKCNQ1OT1 was significantly overexpressed in BC tissue and cell lines. KCNQ1OT1 depletion repressed cell proliferation, migration and invasion, whereas encouraged cell apoptosis. KCNQ1OT1 was a negatively/positively correlated with miR-145-5p/PCBP2 in respect with expression. Mechanically, KCNQ1OT1 was sponge of miR-145-5p and up-regulated the expression of PCBP2. MiR-145-5p inhibition and PCBP2 up-regulation could countervail the tumor-inhibitor role of KCNQ1OT1 knockdown in BC.ConclusionKCNQ1OT1 serves as competing endogenous RNA (ceRNA) to up-regulate PCBP2 via sponging miR-145-5p in BC progression.
Highlights
The large involvement of long non-coding RNAs (LncRNAs) in the biological progression of numerous cancers has been reported
We observed that knockdown of KCNQ1OT1 significantly crippled bladder cancer (BC) cell viability (Fig. 1d)
terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) examined the influence of sh-KCNQ1OT1 in cell apoptosis
Summary
The large involvement of long non-coding RNAs (LncRNAs) in the biological progression of numerous cancers has been reported. The function of lncRNA KCNQ1OT1 in bladder cancer (BC) remains largely unknown. Long non-coding RNAs (lncRNAs) refer to those genes with exceeding 200 nucleotides (nt) in length but without the capacity to encode proteins [5]. LncRNAs have been reported to be abnormally expressed in various cancers, and exerts an irreplaceable function in the carcinogenesis and progression of malignancies [6,7,8,9,10,11]. LncRNAs are associated with different pathological cellular processes, such as cell proliferation, apoptosis, invasion as well as migration. LncRNA SNHG1 regulates colorectal cancer epithelial-mesenchymal transition (EMT) process and impacts cell activity
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