Oxidative stress-mediated epigenetic remodeling, metastatic progression and cell signaling in cancer

Abstract

Abstract Cancer is a serious public health issue and cases are rising at a high rate around the world. Altered production of reactive oxygen species (ROS) causes oxidative stress (OS) which plays a vital role in cancer development by disrupting signaling pathways and genomic integrity in the cellular microenvironment. In this study, we reviewed the regulation of noncoding RNAs, histone modifications, and DNA methylation which OS is involved in. These mechanisms promote cancer growth, metastasis, and resistance to chemotherapeutic agents. There is significant potential to improve patient outcomes through the development of customized medications and interventions that precisely address the role of OS in the onset and progression of cancer. Redox-modulating drugs, antioxidant-based therapies, and measures to restore regular cellular activity and OS-modulated signaling pathways are some examples of these strategies. One other hypothesis rationalizes the cancer-suppressing effect of OS, which acts as a two-edged condition that warns against the use of antioxidants for cancer treatment and management. The present study was executed to review the impact of OS on epigenetic machinery, the evolution of metastatic cancer, and how OS mediates cellular signaling. Along with, insights into the potential of targeting OS-mediated mechanisms for cancer therapy.