METTL3 facilitates immunosurveillance by inhibiting YTHDF2-mediated NLRC5 mRNA degradation in endometrial cancer.

ABSTRACT:

Background

N6-methyladenosine (m6A) methylation is the most abundant chemical posttranscriptional modification of mRNA, and it is associated with the regulation of the immune response to tumors. However, the function of m6A modification in the immune response to endometrial cancer (EC) remains unknown. Our study investigated the immunological role of methyltransferase-like 3 (METTL3) in EC and the underlying molecular mechanism.

Methods

We investigated the correlation between the expression of METTL3 and CD8 by using an endometrial tissue microarray cohort. Next, we investigated the role and mechanism of METTL3 in the immune response to EC using a mouse tumor model and a CD8⁺ T cell-EC cell coculture system after METTL3 overexpression or depletion. Additionally, R

SUBMITTER: Zhan L 

PROVIDER: S-EPMC10122371 | biostudies-literature | 2023 Apr

REPOSITORIES: biostudies-literature