Long noncoding RNA PCA3 regulates glycolysis, viability and apoptosis by mediating the miR-1/CDK4 axis in prostate cancer. Issue 66 (8th November 2018)

• Record Type: Journal Article
• Authors: Gu, Shuo; Niu, Xiaobing; Mao, Fei; Xu, Zongyuan
• Is Part Of: RSC advances. Volume 8:Issue 66(2018)
• Page Start: 37564
• Page End: 37572
• Publication Date: 2018-11-08
• Subjects: Chemistry -- Periodicals; 540.5
• DOI: 10.1039/c8ra08083f
• Languages: English
• ISSNs: 2046-2069

Abstract

Abstract : We proved that PCA3 regulated aerobic glycolysis, viability and apoptosis by regulating the miR-1/CDK4 axis in prostate cancer cells. Abstract : Prostate cancer is one of the common tumor malignancies in men worldwide. Although long noncoding RNAs (lncRNAs) have been demonstrated to play essential roles in the progression of prostate cancer, the roles and potential mechanism of lncRNA prostate cancer antigen 3 (PCA3) remain poorly understood. In the present study, we investigated the role of PCA3 in aerobic glycolysis, viability and apoptosis in prostate cancer cells and probed the interaction between PCA3 and microRNA-1 (miR-1)/cyclin-dependent kinase 4 (CDK4). Here we found that PCA3 and CDK4 were up-regulated while miR-1 was down-regulated in prostate cancer tissues and cells. Moreover, knockdown of PCA3 inhibited aerobic glycolysis and viability and induced apoptosis in prostate cancer cells. Intriguingly, PCA3 was bound to miR-1 and inhibition of miR-1 reversed the regulatory effect of PCA3 knockdown on aerobic glycolysis, viability and apoptosis in prostate cancer cells. Besides, CDK4 was indicated as a target of miR-1 and it was regulated by PCA3 through functioning as a competing endogenous RNA (ceRNA) of miR-1 in prostate cancer cells. The results indicated that PCA3 might drive aerobic glycolysis, viability and apoptosis by regulating the miR-1/CDK4 axis in prostate cancer cells, providing a promising avenue for treatment of prostate cancer.