An Alternatively Spliced Variant of METTL3 Mediates Tumor Suppression in Hepatocellular Carcinoma.

ABSTRACT: Many post-transcriptional mRNA processing steps play crucial roles in tumorigenesis and the progression of cancers, such as N6-methyladenosine (m⁶A) modification and alternative splicing. Upregulation of methyltransferase-like 3 (METTL3), the catalytic core of the m⁶A methyltransferase complex, increases m⁶A levels and results in significant effects on the progression of hepatocellular carcinoma (HCC). However, alternative splicing of METTL3 has not been fully investigated, and the functions of its splice variants remain unclear. Here, we analyzed both our and online transcriptomic data, obtaining 13 splice variants of METTL3 in addition to canonical full-length METTL3-A in HCC cell lines and tissues. Validated by RT-qPCR and Western blotting, we found that

SUBMITTER: Xu RY 

PROVIDER: S-EPMC9031889 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature