Long non‑coding RNA PCAT6 regulates bladder cancer progression via the microRNA‑143‑3p/PDIA6 axis
- Yuanjie Zhang
- Lin Chen
- Gang Luo
Affiliations: Department of Urology, Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430014, P.R. China
- Published online on: July 1, 2021 https://doi.org/10.3892/etm.2021.10379
Copyright: © Zhang
et al. This is an open access article distributed under the
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Although long non‑coding (lnc)RNAs have been reported to be involved in the pathological development of bladder cancer, the functions of lncRNA prostate cancer‑associated transcript 6 (PCAT6) and its underlying mechanism of action in bladder cancer remain unknown. The present study aimed to investigate the effect of PCAT6 in bladder cancer progression and explore its potential application as a novel treatment target. The expression of PCAT6 and miR‑143‑3p in bladder cancer tissues, adjacent normal tissues and cell lines was measured using reverse transcription‑quantitative PCR. Fluorescence in situ hybridization assay was used to detect the subcellular localization of PCAT6. MTT, EdU, Transwell and wound healing assays were conducted to assess the biological function of PCAT6 on cell proliferation, migration and invasion. Putative binding sites between miR‑143‑3p and PCAT6 or PDIA6 were predicted using starBase, Lncbase and TargetScan analyzes. Dual‑luciferase reporter assay was also used to confirm the potential binding between PCAT6 and miR‑143‑3p. RNA immunoprecipitation assay was performed to verify the possible interaction between PCAT6 and miR‑143‑3p. Western blotting was used to measure the expression of PDIA6. The results demonstrated that the expression levels of PCAT6 were upregulated in bladder cancer tissues relative to those in adjacent normal bladder tissues. Knockdown of PCAT6 served a role in suppressing the proliferation, migration and invasion of T24T and EJ bladder cancer cells. PCAT6 knockdown contributed to a reduction of PDIA6 expression at the mRNA and protein levels compared with that in negative control‑transfected cells, whilst the miR‑143‑3p inhibitor partially mitigated this reduction effect. In addition, rescue experiments revealed that the miR‑143‑3p inhibitors reversed the effects of PCAT6 silencing on the malignant phenotypes of bladder cancer. Collectively, the results of the present study demonstrated that PCAT6 may serve an oncogenic role in bladder cancer via the miR‑143‑3p/PDIA6 axis. These results may provide a potential therapeutic target for the treatment of bladder cancer.