Retracted Article: Long noncoding RNA PCA3 regulates glycolysis, viability and apoptosis by mediating the miR-1/CDK4 axis in prostate cancer.

Retracted Article: Long noncoding RNA PCA3 regulates glycolysis, viability and apoptosis by mediating the miR-1/CDK4 axis in prostate cancer.
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DOI:
10.1039/c8ra08083f
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发表时间:
2018-11-07
期刊:
影响因子:
3.9
通讯作者:
Xu, Zongyuan
Xu, Zongyuan
中科院分区:
化学3区
文献类型:
--
作者:
Gu, Shuo;Niu, Xiaobing;Mao, Fei;Xu, Zongyuan

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前列腺癌是全世界男性常见的恶性肿瘤之一。尽管长非编码RNA(lncRNA)已被证明在前列腺癌的进展中发挥重要作用,但lncRNA前列腺癌抗原3(PCA3)的作用和潜在机制仍知之甚少。在本研究中,我们研究了 PCA3 在前列腺癌细胞有氧糖酵解、活力和凋亡中的作用,并探讨了 PCA3 与 microRNA-1 (miR-1)/细胞周期蛋白依赖性激酶 4 (CDK4) 之间的相互作用。在这里,我们发现前列腺癌组织和细胞中 PCA3 和 CDK4 上调,而 miR-1 下调。此外,PCA3 的敲低会抑制前列腺癌细胞的有氧糖酵解和活力,并诱导细胞凋亡。有趣的是,PCA3 与 miR-1 结合,抑制 miR-1 逆转了 PCA3 敲低对前列腺癌细胞有氧糖酵解、活力和凋亡的调节作用。此外,CDK4被认为是miR-1的靶标,并且它在前列腺癌细胞中作为miR-1的竞争性内源RNA(ceRNA)而受到PCA3的调节。结果表明,PCA3可能通过调节前列腺癌细胞中的miR-1/CDK4轴来驱动有氧糖酵解、活力和细胞凋亡,为前列腺癌的治疗提供了一条有希望的途径。我们证明 PCA3 通过调节前列腺癌细胞中的 miR-1/CDK4 轴来调节有氧糖酵解、活力和细胞凋亡。
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. We proved that PCA3 regulated aerobic glycolysis, viability and apoptosis by regulating the miR-1/CDK4 axis in prostate cancer cells.
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