Developing Combined Modality Therapy with Mitochondria-Targeting Strategy

Numerous molecular and cellular events are associated with the development of resistance to chemotherapy or radiotherapy, such as deregulation of the cell cycle, inhibition of DNA damage repair mechanisms, and metabolic alterations. Most cancer therapy-induced responses, including resistance, involve the dysfunction of mitochondria. Mitochondria have acquired numerous functions over the course of evolution, such as those involved in controlling energy production, cellular metabolism, cell survival, apoptosis and autophagy within host cells. Tumor cells can develop defects in mitochondrial function, presenting a potential strategy for designing selective anticancer therapies. However, non-specifically targeting mitochondrial functions may have major unwarranted effects in cancer treatment, including the suppression of normal cell growth and survival. Therefore, treatments conjugated with other anticancer therapy are needed to precisely target specific mitochondrial proteins that are involved in tumor progression and the acquisition of cancer resistance.

In this article collection, we welcome contributions of original research articles, reviews, or shorter “perspective” articles on all aspects related to the theme of “Developing combined modality therapy with mitochondria-targeting strategy ". We hope to highlight current research progression, trends, and challenges with functional insights of emerging mitochondria targets that are associated with cancer response to clinical treatments from a cellular and molecular perspective. The findings regarding mitochondria-targeted agents, as well as the potential application and therapeutic benefit in cancer therapy also fall within the aims and scope of this Special Issue.