RNA N6-methyladenosine (m6A) promotes epigenetic silencing of tumor suppressor genes in HCC.
Our study on METTL3 deregulation and m6A mediated tumor suppressor gene silencing in HCC is published in Hepatology. Congratulation to Maggie!!
mRNA N6-methyladenosine (m6A) emerges as a new layer of epigenetic regulation. In this study, we showed that the major RNA N6-adenosine methyltransferase, METTL3, was frequently up-regulated and function as an oncogene in human HCC. We further demonstrated that up-regulation of METTL3 resulted in m6A and YTHDF2 dependent epigenetic silencing of tumor suppressor gene, SOCS2 in human HCC. Our findings provided the first proof-of-concept model to illustrate that m6A hypermethylation is a novel mechanism for tumor suppressor gene inaction in human cancers.
Congratulate to Maggie, this paper has been recognized as a top 20 most read paper in Hepatology in 2017-2018
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