Apelin promotes proliferation, migration, and angiogenesis in bladder cancer by activating the FGF2/FGFR1 pathway.
10.12122/j.issn.1673-4254.2025.06.18
- Author:
Wei SU
1
;
Houhua LAI
2
;
Xin TANG
1
;
Qun ZHOU
1
;
Yachun TANG
1
;
Hao FU
1
;
Xuancai CHEN
1
Author Information
1. Department of Urology, Affiliated Nanhua Hospital of Nanhua University, Hengyang 421001, China.
2. Department of Urology, Zhujiang Hospital, Southern Medical University, Guangzhou 510260, China.
- Publication Type:Journal Article
- Keywords:
FGF2/FGFR1 pathway;
J82 cells;
angiogenesis;
apelin;
bladder cancer
- MeSH:
Humans;
Urinary Bladder Neoplasms/blood supply*;
Receptor, Fibroblast Growth Factor, Type 1/metabolism*;
Cell Proliferation;
Cell Movement;
Fibroblast Growth Factor 2/metabolism*;
Neovascularization, Pathologic;
Human Umbilical Vein Endothelial Cells;
Cell Line, Tumor;
Signal Transduction;
Apelin;
Intercellular Signaling Peptides and Proteins/genetics*;
Female;
Male;
Angiogenesis
- From:
Journal of Southern Medical University
2025;45(6):1289-1296
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVES:To investigate the role of apelin in regulating proliferation, migration and angiogenesis of bladder cancer cells and the possible regulatory mechanism.
METHODS:GEO database was used to screen the differentially expressed genes in bladder cancer tissues and cells. Bladder cancer and paired adjacent tissues were collected from 60 patients for analysis of apelin expressions in relation to clinicopathological parameters. In cultured bladder cancer J82 cells and human umbilical vein endothelial cells (HUVECs), the effects of transfection with an apelin-overexpressing plasmid or specific siRNAs targeting apelin, fibroblast growth factor 2 (FGF2) and fibroblast growth factor receptor 1 (FGFR1) on proliferation and migration of J82 cells and tube formation in HUVECs were examined using plate cloning assay, Transwell assay, and angiogenesis assay; the changes in FGF2 expression and FGFR1 phosphorylation were detected using Western blotting.
RESULTS:The expression level of apelin was significantly higher in bladder cancer tissues than adjacent tissues, and bladder cancer cell lines (T24 and J82) also expressed higher mRNA and protein levels of apelin than SV-HUC-1 cells. Apelin expression level in bladder cancer tissues was correlated with tumor invasion, distant metastasis and advanced TNM stages. Apelin knockdown significantly suppressed proliferation and migration of J82 cells and decreased the total angiogenic length of HUVECs. In contrast, apelin overexpression significantly promoted proliferation and migration and enhanced FGFR1 phosphorylation in J82 cells, and increased the total angiogenesis length in HUVECs, but this effects were effectively mitigated by transfection of the cells with FGF2 siRNA or FGFR1 siRNA.
CONCLUSIONS:High expression of apelin promotes J82 cell proliferation and migration and HUVEC angiogenesis by promoting activation of the FGF2/FGFR1 pathway.
