Affiliation:
1. The First Affiliated Hospital of Xinjiang Medical University
2. Southwest Medical University
3. The Affiliated Hospital of Southwest Medical University
Abstract
Abstract
Purpose: To investigate the function of CXCL5 in esophageal squamous cell carcinoma (ESCC) development in vivo and in vitro.
Methods: The expression levels of CXCL5 in ESCC tissues and adjacent tissues were detected in immunohistochemistry (IHC), and the relationship between CXCL5 expression in cancer tissues and clinicopathologic parameters was analyzed. Survival, differential and enrichment analyses were performed in the TCGA cohort. Protein expression of CXCL5 was detected by western blot (WB). Proliferation, migration and invasion of ESCC cells were detected by CCK-8, plate cloning and transwell in vitro. Further validation of CXCL5 function in vivo was performed by nude mouse experiments.
Results: The expression intensity of CXCL5 in cancer tissues was higher than that in adjacent tissues (c2=13.434, P=0.000), confirming that the expression of CXCL5 was up-regulated in ESCC tissues. CXCL5 expression level was statistically correlated with lymph node metastasis of ESCC (c2=13.697, P=0.000), but not with age, gender, tumor size, degree of differentiation, and distant metastasis (P>0.05). Overexpression of CXCL5 significantly increased tumor proliferation, colony formation, migration, invasion, and in vitro, increased the epithelial mesenchymal transition (EMT) and CD44 of ESCC cells, and promoted tumor growth in vitro and in vivo through the STAT3 pathway.
Conclusion: CXCL5 expression was up-regulated and predicted poor prognosis in ESCC. Overexpression of CXCL5 was found to promote the proliferation, migration, invasion, and EMT process of ESCC through the STAT3 pathway. Taken together, CXCL5 may be an oncogenic gene in ESCC.
Publisher
Research Square Platform LLC