CXCL5, the upregulated chemokine in patients with uterine cervix cancer, in vivo and in vitro contributes to oncogenic potential of Hela uterine cervix cancer cells

• Published in: Biomedicine & pharmacotherapy 2018-11, Vol.107, p.1496-1504
• Main Authors: Feng, Xiaona, Zhang, Danfeng, Li, Xinyi, Ma, Shuxia, Zhang, Chunbin, Wang, Jingtao, Li, Yue, Liang, Lichun, Zhang, Pengxia, Qu, Yikun, Zhang, Zeyu, Yang, Zhe, Xiang, Yu, Zhang, Weili, Wang, Shuqiu, Shao, Wenwu, Wang, Weiqun
• Format: Article
• Language: English
• Subjects: Animals; Cell Movement - genetics; Cell Proliferation - genetics; Cervix cancer; Chemokine CXCL5 - genetics; CXCL5; CXCR2; Disease Progression; Female; Gene Expression Regulation, Neoplastic - genetics; HeLa Cells; Humans; Mice; Mice, Nude; Migration; Proliferation; Receptors, Interleukin-8B - genetics; Transplantation, Heterologous; Up-Regulation - genetics; Uterine Cervical Neoplasms - genetics; Uterine Cervical Neoplasms - pathology
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/j.biopha.2018.08.149

•CXCL5 expression is upregulated in tissues of patients with uterine cervix cancer.•CXCL5 contributes tumourigenic process in uterine cervix cancer by autocrine and paracrine pathways.•CXCL5 regulates the gene expression of ERK, p-ERK, AKT, p-AKT, DIABOL, NUMB, NDRG3 and CXCR2. CXCL5 is showed a surprisingly elevated profile and implicated in tumorigenesis in several tumors. However, the expression and function of CXCL5 in uterine cervix cancer (UCC) remain largely unknown. The current study aimed to elucidate the expression pattern of CXCL5 in human UCC tissues and Hela cervix cancer cell, as well as its functions in Hela cells. Our data showed that CXCL5 and its receptor CXCR2 were expressed by Hela uterine cervix cancer cells. CXCL5 was upregulated in UCC tissues, and its overexpression was positively correlated with age, but did not correlate with clinical stages and tumor infiltration. Exogenous administration of CXCL5 and CXCL5 overexpression contributed to proliferation and migration activities of Hela cells in vitro, consistent with this, CXCL5 overexpression also promoted growth of Hela cells in a nude mouse xenograft model. At the gene level, CXCL5 overexpression regulated the expression of tumor-related genes including ERK, p-ERK, AKT, p-AKT, DIABOL, NUMB, NDRG3 and CXCR2. Taken together, CXCL5 may contribute to a dominant role in UCC progression and sever as a potential molecular therapeutic target for UCC.