KIF20A promotes cervical cancer progression by interacting with CLIP1

Cervical Cancer (CC) remains a major cause of cancer-related mortality among women worldwide. Although screening and vaccination have reduced its incidence, advanced-stage cases still pose a serious clinical challenge. This study aimed to identify novel biomarkers and therapeutic targets for CC through integrated bioinformatics and experimental approaches. Analysis of multiple datasets (GSE63514, GSE67522, and TCGA-GTEx) revealed 426 consistently upregulated genes in CC, among which several Kinesin family members, including Kinesin family member 20 A (KIF20A), were significantly overexpressed. KIF20A mRNA and protein levels were markedly elevated in CC patient tissues (n = 306 tumors vs. 22 normal controls). Functional assays demonstrated that KIF20A knockdown strongly inhibited cell proliferation, migration, and tumor growth in vitro and in vivo. Mechanistically, KIF20A interacts with CAP Gly domain containing linker protein 1 (CLIP1) and enhances its protein stability. Rescue experiments confirmed that CLIP1 silencing reversed the oncogenic effects of KIF20A overexpression. These results unveil a previously unrecognized KIF20A-CLIP1 regulatory axis in CC progression and suggest its potential as both a biomarker and a therapeutic target.

Supplementary Information: The online version contains supplementary material available at 10.1038/s41598-026-42883-4.

CLIP1; Cervical cancer; KIF20A; Molecular interaction; Tumor progression.