CDH18 promotes proliferation and migration of cervical cancer cells via the Wnt/β-catenin signaling pathway
10.19405/j.cnki.issn1000–1492.2026.06.017
- VernacularTitle:CDH18通过Wnt/β-catenin信号通路促进宫颈癌细胞增殖和迁移
- Author:
Xuechen ZHANG
1
;
Yangliu DONG
1
;
Bo ZHAO
1
;
Zongyi XIA
1
;
Zhaocheng DONG
1
;
Xiangyi ZHE
1
;
Zhenzhen PAN
2
;
Zemin PAN
1
Author Information
1. School of Medicine / Key Laboratory of Xinjiang Endemic and Ethnic Diseases， Shihezi University， Shihezi 832002
2. Department of Laboratory， Fourth Division Hospital of Xinjiang Production and Construction Corps， Yining 835000
- Publication Type:Journal Article
- Keywords:
CDH18;
cervical cancer;
Wnt/β-catenin signaling pathway;
XAV939;
cell proliferation;
cell migration
- From:
Acta Universitatis Medicinalis Anhui
2026;61(6):1111-1123
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo reveal the effects of overexpression and knockdown of CDH18 gene on cervical cancer proliferation and migration levels through the Wnt/β-catenin signaling pathway in cervical cancer cells. MethodsA comprehensive analysis of CDH18-interacting molecules was performed via the bioinformatics STRING database （http：//cn.string-db.org）. Molecular docking between Wnt/β-catenin inhibitor XAV939 and β-catenin was performed using the bioinformatics tool AutoDock （http：//autodock.scripps.edu）. The effect of CDH18 on β-catenin subcellular distribution was detected by laser confocal microscopy. EdU assay， wound healing assay and Transwell assay were used to detect the effects of CDH18 gene overexpression， CDH18 gene knockdown and the XAV939 on cell proliferation and migration. Western blot was performed to measure the expression levels of Wnt/β-catenin pathway-related molecules， including β-catenin， transcription factor 4 （TCF4）， and cellular myelocytomatosis oncogene （c-Myc）， following CDH18 gene overexpression， CDH18 gene knockdown， or XAV939 treatment. ResultsIn SiHa and HeLa cells， CDH18 gene overexpression significantly increased the protein expression levels of β-catenin， TCF4 and c-Myc， decreased the protein expression of GSK-3β， and enhanced cell proliferation and migration， with statistically significant differences （P<0.05）. Conversely， CDH18 gene knockdown significantly reduced the protein expression of β-catenin， TCF4 and c-Myc， elevated GSK-3β expression， and suppressed cell proliferation and migration （P<0.05）.Treatment with XAV939 in SiHa and HeLa cells downregulated β-catenin， TCF4 and c-Myc， upregulated GSK-3β， and inhibited cell proliferation and migration， with significant differences （P<0.05）. ConclusionCDH18 promotes the proliferation and migration of cervical cancer cells via the Wnt/β-catenin signaling pathway.
