Journal
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
Volume 24, Issue 6, Pages 3521-3533Publisher
WILEY
DOI: 10.1111/jcmm.15042
Keywords
butyrate; CCNE1; colorectal cancer; intestinal microbiota metabolites; m6A; methyltransferase like 3
Categories
Funding
- National Natural Science Foundation of China [81472634, 81572595]
- Priority Academic Program Development of Jiangsu Higher Education Institutions [JX10231801]
- Key Project of Jiangsu Provincial Health [H201110]
- Jiangsu Province's Key Provincial Talents Program [ZDRCA2016089]
- Innovation Capability Development Project of Jiangsu Province
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m6A modification is the most prevalent RNA modification in eukaryotes. As the critical N6-methyladenosine (m6A) methyltransferase, the roles of methyltransferase like 3 (METTL3) in colorectal cancer (CRC) are controversial. Here, we confirmed that METTL3, a critical m6A methyltransferase, could facilitate CRC progression in vitro and in vivo. Further, we found METTL3 promoted CRC cell proliferation by methylating the m6A site in 3 '-untranslated region (UTR) of CCNE1 mRNA to stabilize it. Moreover, we found butyrate, a classical intestinal microbial metabolite, could down-regulate the expression of METTL3 and related cyclin E1 to inhibit CRC development. METTL3 promotes CRC proliferation by stabilizing CCNE1 mRNA in an m6A-dependent manner, representing a promising therapeutic strategy for the treatment of CRC.
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