4.6 Article Retracted Publication

被撤回的出版物: miR-132 inhibits cell proliferation, invasion and migration of hepatocellular carcinoma by targeting PIK3R3 (Retracted article. See vol. 59, 2021)

期刊

INTERNATIONAL JOURNAL OF ONCOLOGY
卷 47, 期 4, 页码 1585-1593

出版社

SPANDIDOS PUBL LTD
DOI: 10.3892/ijo.2015.3112

关键词

hepatocellular carcinoma; microRNA; miR-132; PIK3R3

类别

向作者/读者索取更多资源

MicroRNA-132 (miR-132) has been reported to play a tumor suppressive role in different human malignancies. However, its role and underling mechanism in hepatocellular carcinoma (HCC) remains poorly defined due to lack of target gene information. In the present study, we demonstrated that the mean level of miR-132 in hepatocellular carcinoma (HCC) tissues was significantly lower than that in matched tumor-adjacent tissues, and its expression negatively correlated with tumor differentiation (P<0.01), TNM stage (P<0.01) and lymph node metastasis (P<0.01). Similarly, the expression of miR-132 was obviously reduced in HCC cell lines as compared with a normal hepatic cell line. Ectopic expression of miR-132 inhibited cell proliferation, colony formation, migration and invasion, and induced apoptosis in HepG2 cells. In vivo studies showed that miR-132 inhibited tumor growth of HCC and decreased tumor volume and weight. In addition, phosphoinositide-3-kinase regulatory subunit 3 (PIK3R3) was identified as a direct target of miR-132 by a luciferase reporter assay. Western blot and qRT-PCR analysis indicated that PIK3R3 was significantly downregulated by miR-132 in HCC cells. miR-132 expression inversely correlated with PIK3R3 mRNA expression in clinical HCC tissues. Investigations into possible mechanisms revealed that miR-132 inactivated the AKT/mTOR signaling pathway, which may contribute to inhibition of proliferation, migration, and invasion of HCC. These findings suggested that miR-132 may serve as a potential target in the treatment of human HCC.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.6
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据