M⁶A -mediated lncRNA SCIRT stability promotes NSCLC progression through binding to SFPQ and activating the PI3K/Akt pathway.

ABSTRACT: Non-small cell lung cancer (NSCLC) has emerged as one of the most prevalent malignancies worldwide. N6-methyladenosine (m⁶A) methylation, a pervasive epigenetic modification in long noncoding RNAs (lncRNAs), plays a crucial role in NSCLC progression. Here, we report that m⁶A modification and the expression of the lncRNA stem cell inhibitory RNA transcript (SCIRT) was significantly upregulated in NSCLC tissues and cells. Functional analysis revealed that SCIRT enhanced NSCLC cell proliferation, migration, invasion, and epithelial‒mesenchymal transition. The m⁶A modification of SCIRT can be installed by METTL3, which enhanced the stability of this lncRNA. Notably, SCIRT overexpression in response to DNA double-strand breaks (DSBs) sensitized cells to camptoth

SUBMITTER: Cheng Y 

PROVIDER: S-EPMC11772919 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature