Abstract
A growing body of evidence suggests that microRNA-363 (miR-363) plays crucial roles in tumor progression, development and metastasis, and confer resistance to chemotherapeutic drugs in several types of cancers. However, the biological function and underlying molecular mechanism of miR-363 in hepatocellular carcinoma (HCC) have not been fully elucidated. In the present study, we investigated the biological function and mechanism of miR-363 in the regulation of HCC progression. We found that miR-363 was downregulated in HCC cell lines and tissues, and a low expression level of miR-363 was associated with tumor differentiation, TNM stage and lymph node metastasis. Forced overexpression of miR-363 significantly suppressed HCC cell proliferation, migration, invasion and decreased epithelial‑mesenchymal transition (EMT) invitro, as well as inhibited tumor growth invivo. Analysis of the underlying mechanisms revealed that miR-363 regulated E2F transcription factor3 (E2F3) expression by directly targeting its 3'untranslated region. E2F3 overexpression partially attenuated the tumor-suppressive effects of miR-363 in HCC cells. In addition, E2F3 expression was upregulated in the HCC tissues, and was negatively correlated with the level of miR-363 in human HCC tissues. Taken together, these results revealed that miR-363 is involved in HCC growth and invasion and functions as a tumor suppressor by negatively regulating E2F3.
Highlights
D the biological function and underlying molecular mechanism of miR-363 in hepatocellular carcinoma (HCC) have not been fully elucidated
Emerging evidence suggests that a wide range of miRNAs play crucial roles in the development and progression of HCC, and they act as oncogenes or tumor suppressors in HCC [9,10]
HCC cells by targeting SOX9 [19]. miR-133a suppressed combined with western blotting, we showed that E2F transcription factor 3 (E2F3) is a proliferation, colony formation, migration and invasion of direct target of miR-363 in HCC cells
Summary
As shown miR-363 markedly suppressed E2F3 expression at the mRNA, overexpression of miR-363 resulted in increased and protein levels (Fig. 4C and D) in HepG2 cells. E2F3 expression at the (A) mRNA and (B) protein levels was determined in HepG2 cells transfected with miR-363 with/without the E2F3 overexpression plasmid. T proliferation, colony formation, migration and invasion were determined in HepG2 cells transfected with miR-363 with/without the E2F3 overexpression plasmid; P
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