The transcription factor FOXN3 inhibits cell proliferation by downregulating E2F5 expression in hepatocellular carcinoma cells
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Ji Sun1,2,*, Hong Li2,*, Qi Huo2, Meiling Cui2, Chao Ge2, Fangyu Zhao2, Hua Tian2, Taoyang Chen3, Ming Yao2, Jinjun Li2
1Shanghai Medical College, Fudan University, Shanghai, China
2State Key Laboratrory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China
3Qi Dong Liver Cancer Institute, Qi Dong, Jiangsu Province, China
*These authors contributed equally to this work
Jinjun Li, email: firstname.lastname@example.org
Keywords: FoxN3/CHES1, E2F5, hepatocellular carcinoma
Received: April 04, 2016 Accepted: May 23, 2016 Published: June 02, 2016
Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related death worldwide, and the mechanisms underlying the development of HCC remain to be elucidated. Forkhead box N3 (FOXN3) is an important member of the FOX family of transcription factors that plays an essential role in several cancers but has not been investigated in HCC. In this study, we demonstrate that FOXN3 is downregulated in human primary HCC tissues compared with their matched adjacent liver tissues. Functional tests of FOXN3 demonstrated that FOXN3 inhibits the proliferation of HCC cells in vitro and in vivo. Additionally, FOXN3 repressed the mRNA and protein expression of E2F5, a reported potential oncogene, by inhibiting the promoter activity of E2F5. Collectively, our findings indicate that FOXN3 functions as a tumor suppressor in HCC by downregulating the expression of E2F5.
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