期刊
INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
卷 16, 期 8, 页码 1417-1426出版社
IVYSPRING INT PUBL
DOI: 10.7150/ijbs.42019
关键词
miR-197-3p; prostate cancer; VDAC1; AKT
资金
- National Natural Science Foundation of China [81772573, 81672413]
- Guangzhou Science Technology and Innovation Commission [2016201604030003]
- Young Teacher Foundation of Sun Yat-sen University [17ykpy69]
Accumulating investigations have demonstrated that microRNAs (miRNAs) are promising efficient targets for the next generation of molecular therapeutics. The development of miRNA-based therapies requires the identification and validation of cancer-associated miRNAs. Herein, we identified that miR-197-3p regulates the carcinogenesis and development of prostate cancer (PCa) via ''bioinformatics analysis. Next, we investigated the function and regulatory mechanisms of miR-197-3p in PCa. Overexpression of miR-197-3p suppressed PCa cell proliferation and colony formation. In contrast, inhibition of miR-197-3p activity enhanced PCa cell proliferation and colony formation. Mechanistic investigations identified that voltage dependent anion channel 1 (VDAC1) is a direct target of miR-197-3p. miR-197-3p targeting of VDAC1 resulted in downregulation of p-Akt and 13-catenin. Subsequently, we found that restoration of VDAC1 abolished the effects of miR-197-3p on PCa cell proliferation and AKT signaling pathway. Furthermore, we confirmed that miR-197-3p suppressed tumor xenograft growth in vivo. In conclusion, our study offers an empirical investigation of miR-197-3p, a tumor suppressor that may be a potential therapeutic target in PCa.
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