METTL3-mediated m⁶A mRNA modification promotes esophageal cancer initiation and progression via Notch signaling pathway.

ABSTRACT: Esophageal cancer is a lethal malignancy with a high mortality rate, while the molecular mechanisms underlying esophageal cancer pathogenesis are still poorly understood. Here, we found that the N6-methyladenosine (m⁶A) methyltransferase-like 3 (METTL3) is significantly upregulated in esophageal squamous cell carcinoma (ESCC) and associated with poor patient prognosis. Depletion of METTL3 results in decreased ESCC growth and progression in vitro and in vivo. We further established ESCC initiation and progression models using Mettl3 conditional knockout mouse and revealed that 3METTL3-mediated m⁶A modification promotes ESCC initiation and progression in vivo. Moreover, using METTL3 overexpression ESCC cell model and Mettl3 conditional

SUBMITTER: Han H 

PROVIDER: S-EPMC8416973 | biostudies-literature | 2021 Dec

REPOSITORIES: biostudies-literature