Erratum to: Overcoming Drug Resistance Through Elevation of ROS in Cancer

Abstract

Drug resistance is the most devastating problem in treating cancer and drug-resistant cells are harder to kill with the same drug. The mechanism of drug resistance is believed to differ in various cancers for different anticancer drugs. Most of the anticancer agents induce the generation of Reactive Oxygen Species (ROS) to kill cancer cells by apoptosis. However, prolonged treatment with the same drug reduces the ROS level and this reduced ROS level causes drug-sensitive cancer cells to become drug-resistant. Exogenous ROS in conjunction with the same drug resensitizes these drug-resistant cells. Thus, the apoptosis of cancer cells by inducing ROS generation or drug resistance by lack of ROS could be the principle mechanisms of drug sensitivity or drug resistance in various cancer cells. The genetic mechanism of ROS-induced drug sensitivity and ROS depletion leading to drug resistance in various cancer cells with most of the anticancer drugs could involve ‘common molecular pathways’. Understanding the molecular mechanism of ROS generation and maintenance could identify distinct targets for subsequent manipulation to elevate ROS levels in cancer cells. Thus, a ‘combi- national chemotherapy’ could be designed using an anticancer drug while main- taining an elevated level of ROS in the cell during the drug treatment for developing a successful chemotherapy.