RNA methyltransferase METTL3 induces intrinsic resistance to gefitinib by combining with MET to regulate PI3K/AKT pathway in lung adenocarcinoma.

ABSTRACT: Clinical research data show that gefitinib greatly improves the progression-free survival of patients, so it is used in advanced non-small cell lung cancer patients with EGFR mutation. However, some patients with EGFR sensitive mutations do not have good effects on initial gefitinib treatment, and this mechanism is rarely studied. METTL3, a part of N6-adenosine-methyltransferase, has been reported to play an important role in a variety of tumours. In this study, we found that METTL3 is up-regulated in gefitinib-resistant tissues compared to gefitinib-sensitive tissues. Cell function experiments have proved that under the treatment of gefitinib, METTL3 knockdown promotes apoptosis and inhibits proliferation of lung cancer cells. Mechanistic studies have shown that METTL3 combines with MET a

SUBMITTER: Gao F 

PROVIDER: S-EPMC7933928 | biostudies-literature | 2021 Mar

REPOSITORIES: biostudies-literature