Ye Yafei, Yang Shengnan, Han Yanping, Sun Jingjing, Xv Lijuan, Wu Lina, Wang Yongfeng, Ming Liang
Department of Clinical Laboratory, The First Affiliated Hospital of Zhengzhou University, Henan, Zhengzhou 450000, China.
Aging (Albany NY). 2018 Jun 21;10(6):1523-1533. doi: 10.18632/aging.101488.
Long intergenic non-coding RNA Linc00472 has been considered as a tumor suppressor in some cancers. However, the function and mechanism of Linc00472 in colorectal cancer has not been well elucidated. In this study, we found that Linc00472 was down-regulated in colorectal cancer tissues and cells. Elevated Linc00472 expression suppressed proliferation and induced apoptosis in colorectal cancer cells. Moreover, Linc00472 acted as a competing endogenous RNA (ceRNA) of miR-196a to release programmed cell death 4 (PDCD4). Furthermore, miR-196a overexpression or PDCD4 knockdown reversed Linc00472-mediated proliferation inhibition and apoptosis induction in colorectal cancer cells. Ectopic Linc00472 expression hindered tumor growth . Our study demonstrated that Linc00472 suppressed proliferation and induced apoptosis through up-regulating PDCD4 by decoying miR-196a, which may be an effective therapeutic target for colorectal cancer.
长链基因间非编码RNA Linc00472在某些癌症中被认为是一种肿瘤抑制因子。然而,Linc00472在结直肠癌中的功能和机制尚未得到充分阐明。在本研究中,我们发现Linc00472在结直肠癌组织和细胞中表达下调。Linc00472表达升高可抑制结直肠癌细胞的增殖并诱导其凋亡。此外,Linc00472作为miR-196a的竞争性内源性RNA(ceRNA),可释放程序性细胞死亡蛋白4(PDCD4)。此外,miR-196a过表达或PDCD4敲低可逆转Linc00472介导的结直肠癌细胞增殖抑制和凋亡诱导。异位表达Linc00472可抑制肿瘤生长。我们的研究表明,Linc00472通过诱捕miR-196a上调PDCD4,从而抑制增殖并诱导凋亡,这可能是结直肠癌的一个有效治疗靶点。