南京医科大学学报（自然科学版）2025，Vol.45Issue(11)：1546-1562,17.DOI:10.7655/NYDXBNSN250235
METTL3介导的KIF11 mRNA m6A修饰通过PI3K/AKT信号通路促进结直肠癌进展
METTL3-mediated m6A modification of KIF11 mRNA promotes colorectal cancer progression through the PI3K/AKT signaling pathway
摘要
Abstract
Objective:To investigate the biological functions and molecular regulatory mechanisms of kinesin family member 11(KIF11)in colorectal cancer(CRC).Methods:The expression of KIF11 in CRC was examined by qRT-PCR and public databases.Functional assays(CCK-8,colony formation,EdU,and Transwell)were employed to evaluate KIF11's roles in CRC progression.Western blot,RIP-qPCR,MeRIP-qPCR,and RNA stability assays were performed to elucidate the molecular mechanism of N6-methyladenosine(m6A)modification for KIF11.RNA sequencing(RNA-seq)and correlation analysis were used to examine the downstream mechanism of KIF11 regulation.Results:KIF11 was highly expressed in CRC and promoted CRC proliferation and migration.Mechanistically,methyltransferase-like 3(METTL3)/insulin like growth factor 2 mRNA binding protein 2(IGF2BP2)enhanced KIF11 mRNA stability and expression in an m6A-dependent way.Furthermore,by means of the PROM1/PI3K/AKT pathway,KIF11 facilitated the progression of CRC.Conclusion:The m6A modification of KIF11 by METTL3/IGF2BP2 contributes to CRC progression via the PI3K/AKT signaling pathway,highlighting its potential as a prognostic biomarker and therapeutic target.关键词
结直肠癌/KIF11/m6A/METTL3/PI3K/AKT信号通路Key words
colorectal cancer/KIF11/m6A/METTL3/PI3K/AKT pathway分类
临床医学引用本文复制引用
林书慧,钱萌森,朱静,丁洁,罗茜,李杰,李娟,王娟,王科明..METTL3介导的KIF11 mRNA m6A修饰通过PI3K/AKT信号通路促进结直肠癌进展[J].南京医科大学学报（自然科学版）,2025,45(11):1546-1562,17.基金项目
江苏省卫生健康委员会医学科研重点项目(K2023024) （K2023024）
789 Outstanding Talent Program of SAHNMU(789ZYRC202090147) （789ZYRC202090147）
