LncRNA KCNQ1OT1 facilitates the progression of bladder cancer by targeting MiR-218-5p/HS3ST3B1

• Published in: Cancer gene therapy 2021-04, Vol.28 (3-4), p.212-220
• Main Authors: Li, Yongzhi, Shi, Benkang, Dong, Fengming, Zhu, Xingwang, Liu, Bing, Liu, Yili
• Format: Article
• Language: English
• Subjects: 45/41; 631/208/199; 631/67/589/1863; 82/51; 82/80; 82/81; 96/21; 96/34; 96/95; Animals; Antisense RNA; Apoptosis; Biomedical and Life Sciences; Biomedicine; Bladder cancer; Cancer; Cell Line, Tumor; Cell proliferation; Chromosome 5; Development and progression; Disease Progression; Gene Expression; Gene Therapy; Genetic aspects; Glucosamine; Health aspects; Heparan sulfate; Heterografts; Humans; KCNQ1 protein; KCNQ1OT1 protein; Male; Metastases; Mice; Mice, Inbred BALB C; Mice, Nude; MicroRNAs - genetics; MicroRNAs - metabolism; Non-coding RNA; Oncology, Experimental; Phenotypes; Potassium channels (voltage-gated); Potassium Channels, Voltage-Gated - genetics; Potassium Channels, Voltage-Gated - metabolism; RNA; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism; Sulfotransferase; Sulfotransferases - genetics; Sulfotransferases - metabolism; Transcription; Urinary Bladder Neoplasms - genetics; Urinary Bladder Neoplasms - metabolism
• ISSN: 0929-1903; 1476-5500
• DOI: 10.1038/s41417-020-00211-6

Long non-coding RNA (lncRNA) is characterized by biological function in diverse cancers. LncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) is well acknowledged to regulate various cancers, while its role in bladder cancer remains unclear. In the present study, we aimed at probing into the impact and detailed mechanisms of KCNQ1OT1 in bladder cancer progression. In this study, we demonstrated that KCNQ1OT1 expression in bladder cancer tissues was notably up-regulated compared with in normal adjacent tissues, and KCNQ1OT1 modulated the malignant phenotypes of bladder cancer cells. Moreover, it was validated that KCNQ1OT1 could specifically bind to miR-218-5p and reduce its expression. Overexpressed miR-218-5p would inhibit the proliferation and metastasis of bladder cancer cells while facilitating apoptosis. In terms of Mechanism, Heparan Sulfate-Glucosamine 3-Sulfotransferase 3B1 (HS3ST3B1) was validated as a target gene of miR-218-5p, and could be regulated by KCNQ1OT1 indirectly. In conclusion, KCNQ1OT1 can promote the progression of bladder cancer through regulation of miR-218-5p/HS3ST3B1, which is expected to serve as a new therapeutic target for bladder cancer.