Unveiling Therapeutic Targets: Targeting Mitochondrial ROS for Anticancer Therapy

Despite energy metabolism, apoptosis regulation, and cell signaling; mitochondria are also indispensably accountable for cancer initiation and progression, as affirmed by several studies. Furthermore, mitochondria are the most important site for the generation of reactive oxygen species (ROS), responsible for the preservation of redox balance; its overproduction also endorses cancer growth by modulating gene expressions and participation in various signaling pathways, thereby inducing genomic instability. Since tumor cells have long been found to reveal altered mitochondrial structure and function, thus, targeting mitochondria has emerged as a possible intervention for cancer therapies. Nonetheless, numerous stratagems have been proposed to date for selective delivery to mitochondria. Due to the low efficacy and toxicities of currently using mitochondria-targeting anticancer agents as an effective anticancer therapy, mitochondria-targeting nanotechnologies have emerged as a novel approach that has been demonstrated to be effective in cancer therapies in both in vitro and in vivo studies. Currently, numerous types of nanomaterials including polymeric, lipid, metallic, magnetic, silica, semiconductor, and graphene oxide nanoparticles have been fabricated for mitochondria-targeted cancer therapies to augment cancer cell destruction. In consistent, the present book chapter aims to abridge the possible role of mitochondrial ROS on cancer progression and gives a summary of the possibilities to target mitochondria for anticancer therapies.