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深入了解 LINC00152/miR-215/CDK13 轴在肝癌进展中的分子机制。

Insight into the molecular mechanism of LINC00152/miR-215/CDK13 axis in hepatocellular carcinoma progression.

机构信息

Department of Hepatobiliary Surgery, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, Guangxi, China.

Clinic Medicine Research Center for Hepatobiliary Diseases, The Affiliated Hospital of Youjiang Medical University for Nationalities, Guangxi, China.

出版信息

J Cell Biochem. 2019 Nov;120(11):18816-18825. doi: 10.1002/jcb.29197. Epub 2019 Jul 11.

DOI:10.1002/jcb.29197
PMID:31297882
Abstract

Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in the world. Nevertheless, its underlying molecular mechanisms are largely unknown. LINC00152 are recently investigated in several cancer types. In our current investigation, we observed LINC00152 was obviously upregulated in HCC cells. LINC00152 was significantly downregulated by infecting LV-shLINC00152 in HepG2 and SNU449 cells. Loss of LINC00152 remarkably repressed HCC cell proliferation, cell colony formation, induced cell apoptosis, and restrained cell migration/invasion. Growing evidence has reported long noncoding RNAs can sponge microRNAs to modulate cancer process. Here, we indicated miR-215 was greatly decreased in HCC and LINC00152 regulated HCC development via sponging miR-215. For another, the binding association between LINC00152 and miR-215 was proved by a series of functional assays. CDK13 was predicted as the target of miR-215. Upregulation of miR-215 greatly depressed CDK13 in HCC cells. Subsequently, the in vivo results demonstrated that silence of LINC00152 restrained HCC development via modulating miR-215 to up-regulate CDK13. Therefore, it was revealed that LINC00152 contributed to the progression of HCC by the modulation of miR-215 and CDK13.

摘要

肝细胞癌 (HCC) 是世界上最常见的恶性肿瘤之一。然而,其潜在的分子机制在很大程度上尚不清楚。LINC00152 最近在几种癌症类型中得到了研究。在我们目前的研究中,我们观察到 LINC00152 在 HCC 细胞中明显上调。通过感染 HepG2 和 SNU449 细胞中的 LV-shLINC00152,LINC00152 明显下调。LINC00152 的缺失显著抑制了 HCC 细胞的增殖、细胞集落形成,诱导细胞凋亡,并抑制细胞迁移/侵袭。越来越多的证据表明,长非编码 RNA 可以通过海绵 microRNA 来调节癌症进程。在这里,我们表明 miR-215 在 HCC 中显著降低,LINC00152 通过海绵 miR-215 调节 HCC 发展。另一方面,通过一系列功能测定证明了 LINC00152 和 miR-215 之间的结合关联。CDK13 被预测为 miR-215 的靶标。miR-215 在 HCC 细胞中的上调大大抑制了 CDK13。随后,体内结果表明,沉默 LINC00152 通过调节 miR-215 来上调 CDK13 从而抑制 HCC 的发展。因此,研究结果表明,LINC00152 通过调节 miR-215 和 CDK13 促进 HCC 的进展。

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