M⁶A modification enhances the stability of CDC25A promotes tumorigenicity of esophagogastric junction adenocarcinoma via cell cycle.

ABSTRACT: N6-Methyladenosine (m⁶A) modification and its regulators play critical roles in human cancers, but their functions and regulatory mechanisms in adenocarcinoma of the esophagogastric junction (AEG) remain unclear. Here, we identified that IGF2BP3 is the most significantly up-regulated m⁶A regulator in AEG tumors versus paired normal adjacent tissues from the expression profile of m⁶A regulators in a large cohort of AEG patients. Silencing IGF2BP3 inhibits AEG progression in vitro and in vivo. By profiling transcriptome-wide targets of IGF2BP3 and the m⁶A methylome in AEG, we found that IGF2BP3-mediated stabilization and enhanced expression of m⁶A-modified targets, including targets of the cell cycle pathway, such as

SUBMITTER: Pan Y 

PROVIDER: S-EPMC11379066 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature