The epithelial-mesenchymal transition (EMT) plays an important role in the progression of cancer, metastasis and drug resistance. Several factors are known to mediate EMT-driven drug resistance in cancer cells, among them the tumor microenvironment (TME). This phenomenon has gained attention in the field of cancer biology for its potential contribution to in the progression of carcinomas. It is also known that tumor cells experiencing EMT increases the secretion of specific factors in the TME, including cytokines, chemokines and growth factors, which can play an important role in tumor progression. The main event in EMT is the repression of E-cadherin driven by transcriptional factors including SNAIL, SLUG and ZEB1. Chemokines function as growth factors, activating, through its receptor CXCR2 and transcription factors such as SNAIL, thus inducing the EMT phenotype, contributing to the progression of the disease. Studies have investigated how the acquisition of mesenchymal characteristics could contribute to the development of a tumor microenvironment, and point to a possible link between the CXCR2 pathway and EMT. This review describes the mechanism by which CXCR2 is involved in EMT through SNAIL, contributing to progression of cancer and summarizes new advances in the research of EMTassociated CXCR2.
Published Date: 2020-06-26; Received Date: 2020-06-05