Cisplatin resistance in gastric cancer cells is involved with GPR30-mediated epithelial-mesenchymal transition.

In this study, we demonstrated that GPR30 is involved in cisplatin resistance by promoting EMT in gastric cancer. GPR30 knockdown resulted in increased sensitivity of different gastric cancer (GC) cells to cisplatin and alterations in the epithelial/mesenchymal markers. Furthermore, G15 significantly enhanced the cisplatin sensitivity of GC cells while G1 inhibited this phenomenon. In addition, EMT occurred when AGS and BGC-823 were treated with cisplatin. Down-regulation of GPR30 with G15 inhibited this transformation, while G1 promoted it. Taken together, these results revealed the role of GPR30 in the formation of cisplatin resistance, suggesting that targeting GPR30 signalling may be a potential strategy for improving the efficacy of chemotherapy in gastric cancer.
PMID: 32052561 [PubMed - as supplied by publisher]

Source: J Cell Mol Med - February 11, 2020 Category: Molecular Biology Authors: Wang X, Xu Z, Sun J, Lv H, Wang Y, Ni Y, Chen S, Hu C, Wang L, Chen W, Cheng X Tags: J Cell Mol Med Source Type: research