{Reference Type}: Journal Article
{Title}: METTL14 plays an oncogenic role in NSCLC by modulating ferroptosis and the m6A modification of GPX4.
{Author}: Lou Y;Huang K;Xu B;Chen X;
{Journal}: Arch Physiol Biochem
{Volume}: 0
{Issue}: 0
{Year}: 2024 Jul 11
{Factor}: 3.188
{DOI}: 10.1080/13813455.2024.2376813
{Abstract}: <B>UNASSIGNED: </B>N6-methyladenosine (m6A) of RNA is involved in the progression of non-small cell lung cancer (NSCLC).<BR><B>UNASSIGNED: </B>This study investigated the role of METTL14 in NSCLC and the mechanism.<BR><B>UNASSIGNED: </B>Expression levels were assessed by quantitative real-time PCR and ELISA assays. Cells viability was assessed by cell counting kit-8. M6A methylation was analysed by methylated RNA immunoprecipitation (MeRIP), RIP, luciferase assay, and mRNA stability assay.<BR><B>UNASSIGNED: </B>The results showed that METTL14 was highly expressed in NSCLC tissues and cell lines. Knockdown of METTL14 inhibited the cell viability while induced ferroptosis of NSCLC cells. Mechanistically, METTL14 interacts with GPX4, mediates m6A modification of GPX4, enhances its mRNA stability, and upregulates its expression. In addition, IGF2BP1 recognises the m6A-methylated GPX4 and mediates the elevated mRNA stability. Moreover, GPX4 reversed the effects of METTL14 depletion.<BR><B>UNASSIGNED: </B>The METTL14/GPX4 axis promotes NSCLC progression by inhibiting cell ferroptosis through the recognition of m6A modification mediated by IGF2BP1.