Published online Sep 15, 2016. doi: 10.4251/wjgo.v8.i9.673
Peer-review started: March 28, 2016
First decision: May 23, 2016
Revised: June 7, 2016
Accepted: June 27, 2016
Article in press: June 29, 2016
Published online: September 15, 2016
Gastric cancer is the fourth most common cancer and the second leading cause of cancer deaths worldwide. Chemotherapy is one of the major treatments for gastric cancer, but drug resistance limits the effectiveness of chemotherapy, which results in treatment failure. Resistance to chemotherapy can be present intrinsically before the administration of chemotherapy or it can develop during chemotherapy. The mechanisms of chemotherapy resistance in gastric cancer are complex and multifactorial. A variety of factors have been demonstrated to be involved in chemoresistance, including the reduced intracellular concentrations of drugs, alterations in drug targets, the dysregulation of cell survival and death signaling pathways, and interactions between cancer cells and the tumor microenvironment. This review focuses on the molecular mechanisms of chemoresistance in gastric cancer and on recent studies that have sought to overcome the underlying mechanisms of chemoresistance.
Core tip: Although chemotherapy remains one of the primary therapeutic modalities used in the treatment of gastric cancer, chemoresistance limits the effectiveness of chemotherapy and results in treatment failure. The elucidation of the mechanisms of drug resistance will be very helpful for the prediction of sensitivity to chemotherapy and the reversal of drug resistance to improve therapeutic efficacy. The mechanisms of drug resistance have been broadly investigated in recent years. In this review, we summarize the molecular mechanisms of chemoresistance in gastric cancer and discuss the progress in the reversal of drug resistance.