Biochemical and biophysical research communications · 2026
KIF11 drives ovarian cancer progression and cisplatin resistance via the Wnt/β-catenin signaling pathway.
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Zhao Yu, Long Changchun, Zhang Lingyan
Аннотация
BACKGROUND: Ovarian cancer (OC) typically exhibits aggressive growth and is prone to developing cisplatin (DDP) resistance. One of the Kinesin family members KIF11, is a current research hotspot due to its role in cisplatin resistance, although its underlying mechanisms are not yet fully understood.
METHODS: Differentially expressed genes (DEGs) were obtained from TCGA-OV, GSE23391, and GSE29450, from which candidate genes were screened. Applying qRT-PCR and WB, KIF11 expression in OC cell lines was evaluated, followed by loss- and gain-of-function assays. The regulation of cell phenotype by KIF11 knockdown/overexpression was assessed using Transwell assays, CCK-8, flow cytometry, and colony formation assays. LiCl, an activator of the Wnt/β-catenin pathway, and XAV-939, an inhibitor, were applied to examine the regulatory mechanisms. The function related to chemoresistance was studied using a DDP-resistant cell model (SKOV3-DDP).
RESULTS: Four candidate genes (BUB1B, CCNB1, KIF11, KIF23) were significantly upregulated in OC samples. In vitro, KIF11 was highly expressed in OC cell lines. KIF11 silencing suppressed cell growth, increased apoptosis, and induced G2/M arrest, effects that were partially rescued by LiCl, supporting a functional link to the Wnt/β-catenin pathway. KIF11 was upregulated in SKOV3-DDP cells compared with parental SKOV3 cells. While KIF11 overexpression had the opposite effects, which XAV-939 mitigated, KIF11 knockdown decreased viability and colony formation and increased apoptosis.
CONCLUSION: KIF11 can promote the malignant phenotype and DDP resistance of tumor cells by activating the Wnt/β-catenin signaling pathway in OC. Therefore, KIF11 has the potential to serve as a biomarker for predicting OC progression and the efficacy of DDP treatment.
METHODS: Differentially expressed genes (DEGs) were obtained from TCGA-OV, GSE23391, and GSE29450, from which candidate genes were screened. Applying qRT-PCR and WB, KIF11 expression in OC cell lines was evaluated, followed by loss- and gain-of-function assays. The regulation of cell phenotype by KIF11 knockdown/overexpression was assessed using Transwell assays, CCK-8, flow cytometry, and colony formation assays. LiCl, an activator of the Wnt/β-catenin pathway, and XAV-939, an inhibitor, were applied to examine the regulatory mechanisms. The function related to chemoresistance was studied using a DDP-resistant cell model (SKOV3-DDP).
RESULTS: Four candidate genes (BUB1B, CCNB1, KIF11, KIF23) were significantly upregulated in OC samples. In vitro, KIF11 was highly expressed in OC cell lines. KIF11 silencing suppressed cell growth, increased apoptosis, and induced G2/M arrest, effects that were partially rescued by LiCl, supporting a functional link to the Wnt/β-catenin pathway. KIF11 was upregulated in SKOV3-DDP cells compared with parental SKOV3 cells. While KIF11 overexpression had the opposite effects, which XAV-939 mitigated, KIF11 knockdown decreased viability and colony formation and increased apoptosis.
CONCLUSION: KIF11 can promote the malignant phenotype and DDP resistance of tumor cells by activating the Wnt/β-catenin signaling pathway in OC. Therefore, KIF11 has the potential to serve as a biomarker for predicting OC progression and the efficacy of DDP treatment.