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that the m6A methylation of KIF11 mediated by MET⁃
4 Conclusion
TL3 was recognized by IGF2BP2，which in turn impact⁃
ed its expression. Subsequently，through RNA ⁃ seq In conclusion，our study elucidates a novel mecha⁃
analysis，we found that KIF11 promoted CRC progres⁃ nism through which KIF11 regulates colorectal cancer.
sion by enhancing phosphorylation levels of the PI3K/ We demonstrate that METTL3/IGF2BP2 modulates
AKT pathway. Previous studies have shown that KIF11 KIF11 expression in an m6A⁃dependent manner，influ⁃
also enhances the chemosensitivity of CRC to oxaliplat⁃ encing its stability and thereby regulating PROM1 and
［43］
in through p53/GSK3β signaling . Aberrant activa⁃ activating the PI3K/AKT signaling pathway to facili⁃
tion of the PI3K/AKT pathway regulates autophagy and tate CRC progression. These findings underscore the
EMT levels，induces tumor cell proliferation and migra⁃ potential of KIF11 as a promising predictive biomarker
tion，and also allows tumor cells to evade apoptosis by and an effective therapeutic target，offering new in⁃
creating a dysregulation between anti⁃apoptotic and pro sights into the diagnosis and treatment of CRC.
［44］ 利益冲突声明：
⁃ apoptotic genes . Our study demonstrated that
所有作者声明无利益冲突。
METTL3 silencing considerably attenuated the phos⁃
Conflicts of Interests：
phorylation levels of PI3K and AKT，while overexpres⁃
The authors declare no conflict of interests.
sion of KIF11 in METTL3 ⁃ knockdown cells partially
作者贡献声明：
recovered their phosphorylation levels. These results
林书慧完成实验验证和初稿撰写；朱静负责研究构思和
support the idea that METTL3/IGF2BP2 promotes 实验设计；钱萌森和丁洁完成数据整理与分析；丁洁和李娟
CRC progression through KIF11 by activating the 负责项目资金获取；罗茜和李杰完成数据收集；王科明和王
PI3K/AKT signaling pathway. 娟完成论文的修改与审阅。
Our study also revealed that PROM1 was a down⁃ Author’s Contributions：
stream target of KIF11. Overexpression of PROM1 in LIN Shuhui completed the experimental verification and
initial draft writing；ZHU Jing was responsible for research con⁃
KIF11 ⁃ knockdown cells could rescue the inhibitory
ception and experimental design；QIAN Mengsen and DING Jie
effect of KIF11 on CRC proliferation and migration. In
performed the data organization and analysis；DING Jie and LI
addition，KIF11 was able to promote CRC progression
Juan managed the project funding acquisition；LUO Qian and LI
through the PROM1/PI3K/AKT pathway.
Jie carried out the data collection；WANG Keming and WANG
Despite these conclusions drawn from our study， Juan completed the paper revision and review.
several limitations remain. First，while we have estab⁃
［References］
lished that METTL3 mediates the m6A methylation
［1］ BRAY F，LAVERSANNE M，SUNG H，et al. Global can⁃
modification of KIF11，we have not experimentally
cer statistics 2022：GLOBOCAN estimates of incidence
identified the specific m6A modification sites. Second，
and mortality worldwide for 36 cancers in 185 countries［J］.
although we have recognized the PROM1/PI3K/AKT
CA Cancer J Clin，2024，74（3）：229-263
pathway as a downstream target of KIF11，the precise ［2］ SIEGEL R L，MILLER K D，FUCHS H E，et al. Cancer
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acknowledge as a limitation that multiple testing cor⁃
［4］ GUO X H，ZHOU L，WU Y N，et al. KIF11 as a potential
rections such as the Bonferroni or Benjamini⁃Hochberg
pan ⁃ cancer immunological biomarker encompassing the
procedures were not applied in the current analysis. In
disease staging，prognoses，tumor microenvironment，and
our future research，we will expand the sample size and
therapeutic responses［J］. Oxid Med Cell Longev，2022，
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tistical power and further improve the reliability of our ［5］ DANG W，BIAN R，FAN Q Q，et al. KIF11 promotes cell
research conclusions. Therefore，we will continue our proliferation via ERBB2/PI3K/AKT signaling pathway in
experiments to refine this investigation. gallbladder cancer［J］. Int J Biol Sci，2021，17（2）：514-