Abstract

Aberrant expression of RORγ is implicated in cancer development. A previous study identified that RORγ functions as a tumor promoter to drive hepatocellular carcinoma (HCC) growth. However, its expression and significance in HCC remain unclear. The central finding of this work is that RORγ was overexpressed in HCC due to its dysfunction of promoter methylation, and hepatitis B virus X protein (HBx) can remarkably induce the expression of RORγ in hepatocellular carcinoma through enhancing the transcriptional function. Also, the HBx-induced RORγ could promote the migration and proliferation of hepatoma cells. Hence, these results suggest that RORγ was an important regulator in HCC, and our finding provides new insights into the significance of RORγ in HCC.

Highlights

  • IntroductionThe explanation of different functions in cancers may be due to the tumor microenvironment, and the study of RORc in cancers is worthy of further research

  • BioMed Research International correlation with melanoma progression [16]

  • RORct as a truncated variant was reported overexpressed in peripheral blood mononuclear cells of Hepatocellular carcinoma (HCC) patients. en, we examined the RORc expression of liver cancer

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Summary

Introduction

The explanation of different functions in cancers may be due to the tumor microenvironment, and the study of RORc in cancers is worthy of further research. RORct was reported to be overexpressed in peripheral blood mononuclear cells of HCC patients [18], and the contribution of RORc in HCC still has not been reported. We firstly examined the expression of RORc in HCC and evaluated the potential mechanism. To formulate the hypothesis, we examined the expression of RORc in the tumor and adjacent tissues and found the hypomethylation of RORc in the liver tumor, and RORc expression was further enhanced in the HCC patients with HBV infection. E most important work is that HBx could induce RORc expression by promoting its transcriptional function. E biological function study demonstrated overexpression of RORc can enhance the migration and growth activity of liver cancer cells. Our finding provides new insights into the role of RORc in HCC

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