The pathological roles and potential mechanisms of vascular endothelial growth factor receptor-3 in gastric cancer.

Autor:	Li XF; Department of Pathology, Weifang People's Hospital, the First Affiliated Hospital of Weifang Medical College, Weifang, Shandong Province, China., Zhang XJ; Department of Gynaecology and Obstetrics, the Affiliated Hospital of Maternal and Child Health, Weifang Medical College, Weifang Maternal and Child Health Care Hospital, Weifang, Shandong Province, China., Hao FR; Department of Radiation Oncology, Weifang People's Hospital, the First Affiliated Hospital of Weifang Medical College, Weifang, Shandong Province, China., Dong XT; Department of Pathology, Weifang People's Hospital, the First Affiliated Hospital of Weifang Medical College, Weifang, Shandong Province, China., Xu GD; Department of Pathology, Weifang People's Hospital, the First Affiliated Hospital of Weifang Medical College, Weifang, Shandong Province, China., Zhang YX; Department of Pathology, Weifang People's Hospital, the First Affiliated Hospital of Weifang Medical College, Weifang, Shandong Province, China.
Jazyk:	angličtina
Zdroj:	The Journal of international medical research [J Int Med Res] 2024 Mar; Vol. 52 (3), pp. 3000605241234558.
DOI:	10.1177/03000605241234558
Abstrakt:	Objective: To investigate the roles and underlying mechanisms of vascular endothelial growth factor receptor-3 (VEGFR-3) in gastric cancer (GC). Methods: VEGFR-3 gene expression profiles in human gastric adenocarcinoma (GAC) tissues were analysed using The Cancer Genome Atlas database. Human GC cell lines and were used for in vitro studies. Mouse models of GC and distant metastasis were used for in vivo studies. Silencing of VEGFR-3 gene expression was achieved using small interfering RNA. Results: VEGFR-3 gene expression was significantly elevated in GAC tissues and GC cells. Higher VEGFR-3 expression was positively correlated with more advanced stages and a greater number of metastatic lymph nodes. In vitro studies in GC cells showed that knockdown of VEGFR-3 gene expression significantly suppressed cell proliferation and migration, but promoted apoptosis. In vivo investigations revealed that silencing of VEGFR-3 gene expression exhibited significant inhibition on tumour growth and metastasis. Further mechanistic studies showed that VEGFR-3 exerted its pathological roles by affecting the key molecules in the apoptotic and epithelial-mesenchymal transition pathways. Conclusion: The molecular pathways associated with VEGFR-3-mediated pathological effects could be targets in the development of novel approaches for the diagnosis, prognosis and treatment of GC. Competing Interests: Declaration of conflicting interestThe authors declare that there are no conflicts of interest.
Databáze:	MEDLINE
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