The Expression And Mechanism Of Chemokine CXCL3 In Cervical Cancer HeLa Cells

Objective:To investigate the expression of chemokine CXCL3 in cervical cancer tissues and HeLa cervical cancer cells,and to investigate the effect of overexpression of chemokine CXCL3 on the malignant phenotypes of HeLa cervical cancer cells via autocrine and paracrine pathways and its mechanism of action.Methods:The expression of CXCL3 in cervical tissue microarrays(including 41 cervical tissues and 39 normal cervical tissues)was studied by immunohistochemistry;HeLa cervical cancer cell lines overexpressing chemokine CXCL3 and WPMY-1 were constructed by viral transfection.Interstitial cell line;CCK-8,Transwell experimental study of CXCL3 autocrine and paracrine pathway on the proliferation and migration of HeLa cervical cancer cells;xenotransplantation experiment to study the effect of HeLa overexpression CXCL3 on nude mice transplantation;Western Blot;The effect of HeLa cells overexpressing CXCL3 on the expression of tumor-associated proteins was tested.Results:Immunohistochemistry results showed that the expression of chemokine CXCL3 in cervical cancer tissue was significantly higher than that in normal cervical tissue,and the expression level of CXCL3 was positively correlated with the clinical stage of cervical cancer.CCK-8 and Transwell experimental results showed that HeLa cells overexpressing CXCL3 and conditioned medium of WPMY-1 cells overexpressing CXCL3 cultured HeLa cells can promote the proliferation and migration of HeLa cells.The results of in vivo experiments show that overexpression of CXCL3 can significantly promote HeLa cells in the naked the growth in mice;Western Blot results showed that compared with empty vector transfected cell lines,CXCL3 overexpression HeLa cell lines ERK,p-ERK,Bcl-2 expression levels increased significantly;while Bax expression levels were significantly reduced.Conclusion:The expression of chemokine CXCL3 is up-regulated in cervical cancer tissues.It can promote the malignant phenotype of cervical cancer through the regulation of autocrine and paracrine pathways and the expression of genes involved in the malignant development of tumors.