Dysfunction of IKZF1/MYC/MDIG axis contributes to liver cancer progression through regulating H3K9me3/p21 activity View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-05-04

AUTHORS

Qi Huo, Chao Ge, Hua Tian, Ji Sun, Meiling Cui, Hong Li, Fangyu Zhao, Taoyang Chen, Haiyang Xie, Ying Cui, Ming Yao, Jinjun Li

ABSTRACT

MDIG is known to be overexpressed in many types of human cancers and has demonstrated predictive power in the prognosis of cancer, although the functions and mechanisms of MDIG in liver cancer, especially in hepatocellular carcinoma (HCC), are still unknown. In this study, we report that MDIG and MYC were negatively regulated by IKZF1. MDIG overexpression substantially promoted HCC cell proliferation, cell migration and spreading, whereas knockdown of MDIG would reverse above-mentioned effect. MDIG effects on tumour cell growth were further demonstrated in a tumour xenograft model. Moreover, MDIG had effects on the level of p21(CIP1/WAF1) via H3K9me3 expression in HCC. MDIG was also found to be closely related to the sorafenib resistance of HCC cells in vitro. Clinically, we found that MDIG was frequently overexpressed in human HCCs (69.7%; n=155) and was significantly associated with histological grade and hepatitis B virus infection. Our findings indicate that MDIG plays an important role in HCC progression via MDIG/H3K9me3/p21(CIP1/WAF1) signalling and serves as a potential therapeutic target. More... »

PAGES

e2766-e2766

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    http://scigraph.springernature.com/pub.10.1038/cddis.2017.165

    DOI

    http://dx.doi.org/10.1038/cddis.2017.165

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1085131110

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/28471446


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