American Association for Cancer Research
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Supplementary Figure 3 from Overexpression of the Transcription Factor MEF2D in Hepatocellular Carcinoma Sustains Malignant Character by Suppressing G2–M Transition Genes

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journal contribution
posted on 2023-03-30, 22:33 authored by Leina Ma, Jia Liu, Limei Liu, Guangjie Duan, Qingliang Wang, Yanmin Xu, Feng Xia, Juanjuan Shan, Junjie Shen, Zhi Yang, Ping Bie, Youhong Cui, Xiu-Wu Bian, Jesus Prieto, Matías A. Avila, Cheng Qian

PDF file - 150K, Supplementary Figures S3: The enriched biological processes or molecular pathways presented by genes significantly affected by MEF2D downregulation in Huh7 cells.



The underlying molecular pathogenesis in hepatocellular carcinoma remains poorly understood. The transcription factor MEF2D promotes survival in various cell types and it seems to function as an oncogene in leukemia. However, its potential contributions to solid cancers have not been explored. In this study, we investigated MEF2D expression and function in hepatocellular carcinoma, finding that MEF2D elevation in hepatocellular carcinoma clinical specimens was associated with poor prognosis. MEF2D-positive primary hepatocellular carcinoma cells displayed a faster proliferation rate compared with MEF2D-negative cells, and silencing or promoting MEF2D expression in these settings limited or accelerated cell proliferation, respectively. Notably, MEF2D-silencing abolished hepatocellular carcinoma tumorigenicity in mouse xenograft models. Mechanistic investigations revealed that MEF2D-silencing triggered G2–M arrest in a manner associated with direct downregulation of the cell-cycle regulatory genes RPRM, GADD45A, GADD45B, and CDKN1A. Furthermore, we identified MEF2D as an authentic target of miR-122, the reduced expression of which in hepatocellular carcinoma may be responsible for MEF2D upregulation. Together, our results identify MEF2D as a candidate oncogene in hepatocellular carcinoma and a potential target for hepatocellular carcinoma therapy. Cancer Res; 74(5); 1452–62. ©2014 AACR.

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