FTO-mediated m6A demethylation of CSF3 suppresses NETosis via downregulation of RLN2 expression in colorectal cancer.

ABSTRACT: CSF3 exerts a significant function in the progression of colorectal cancer (CRC). N6-methyladenosine (m6A) modification is now considered the main driving factor of RNA influence for maintaining homeostasis in cancer cells. Nevertheless, how m6A mediates the role of CSF3 and its influence in pathogenesis of CRC is still elusive. After neutrophil isolation from bone marrow, the purity and survival rate of neutrophils were assessed. Azoxymethane (AOM)/Dextran Sodium Sulfate (DSS) was employed to construct the CRC mice model. Both loss-of-function and gain-of-function experiments were conducted to explore the influence of CSF3 on NETosis and tumorigenesis of CRC in vitro and in vivo. The purity and survival rate of neutrophils were 88.07% and 94.84%, respectively. Overexpression of CSF3 (oe-C

SUBMITTER: Xu J 

PROVIDER: S-EPMC12775115 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature