Mechanism of methyltransferase METTL14 mediating m6A modification and regulating SIRT5 expression to promote ferroptosis and repress gastric cancer progression.

ABSTRACT:

Objectives

Gastric cancer (GC) ranks as the third leading reason of cancer-associated deaths worldwide. This study investigates the mechanism by which the m6A methyltransferase methyltransferase-like 14 (METTL14) enhances ferroptosis and inhibits GC progression through regulation of sirtuin 5 (SIRT5).

Methods

In vitro, AGS cells were treated with pcDNA3.1-METTL14, si-SIRT5 and Ferrostatin-1, while NCI-N87 cells were transfected with si-METTL14. Expression levels of METTL4 and SIRT5 were measured using RT-qPCR and Western blot. GC cell proliferation, migration, and invasion were evaluated through CCK-8, colony formation, and transwell assays. The SRAMP database was used to predict m6A modification sites on SIRT5 mRNA. Interaction between METTL14 and SIRT5 was assessed by RIP

SUBMITTER: Zhang H 

PROVIDER: S-EPMC12613479 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature