RETRACTED ARTICLE: miR-665 promotes hepatocellular carcinoma cell migration, invasion, and proliferation by decreasing Hippo signaling through targeting PTPRB

被引:2
|
作者
Hu, Yuanchang [1 ]
Yang, Chao [1 ]
Yang, Shikun [1 ]
Cheng, Feng [1 ]
Rao, Jianhua [1 ]
Wang, Xuehao [1 ]
机构
[1] Nanjing Med Univ, Chinese Acad Med Sci, Hepatobiliary Liver Transplantat Ctr, Key Lab Living Donor Transplantat,Affiliated Hosp, Nanjing, Jiangsu, Peoples R China
来源
CELL DEATH & DISEASE | 2018年 / 9卷 / 10期
基金
中国国家自然科学基金;
关键词
MICRORNA EXPRESSION; SIZE-CONTROL; PATHWAY; CANCER; METASTASIS; PROTEIN; GROWTH; STATISTICS; DROSOPHILA; INFECTION;
D O I
暂无
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Growing evidence suggests that aberrant microRNA (miRNA) expression contributes to hepatocellular carcinoma (HCC) development and progression. However, the potential role and mechanism of miR-665 in the progression of liver cancer remains largely unknown. Our current study showed that miR-665 expression was upregulated in HCC cells and tissues. High expression of miR-665 exhibited more severe tumor size, vascular invasion and Edmondson grading in HCC patients. Gain- or loss-of-function assays demonstrated that miR-665 promoted cell proliferation, migration, invasion, and the epithelial-mesenchymal transition (EMT) of HCC cells in vitro and in vivo. Tyrosine phosphatase receptor type B (PTPRB) was downregulated in HCC tissues, and was negatively correlated with miR-665 expression. Through western blotting and luciferase reporter assay, PTPRB was identified as a direct downstream target of miR-665. Restoration of PTPRB reverses the effects of miR-665 on HCC migration, invasion, and cell proliferation. A mechanistic study showed that PTPTRB mediated the functional role of miR-665 through regulation of the Hippo signaling pathway. In conclusion, our results suggested that miR-665 was a negative regulator of the PTPRB and could promote tumor proliferation and metastasis in HCC through decreasing Hippo signaling pathway activity, which can be a potential target for HCC treatment.
引用
收藏
页数:13
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