Editorial: Developing combined modality therapy with mitochondria-targeting strategy

• Type of Material: Article
• Authors: Yong Teng, Emory University
• Language: English
• Date: 2023-01-06
• Publisher: FRONTIERS MEDIA SA
• Publication Version: Final Published Version
• Copyright Statement: © 2023 Teng
• License: Creative Commons Attribution 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.3389/fonc.2022.1111724
• Title of Journal or Parent Work: FRONTIERS IN ONCOLOGY
• Volume: 12
• Start Page: 1111724
• End Page: 1111724
• Grant/Funding Information: YT is the inaugural recipient of the Wally Award from Winship Cancer Institute. His research was funded by NIH-NIDCR grants R01DE028351, R03DE028387 and R03DE032084.
• Keywords: Science & Technology; translational sciences; mitochondria and disease; cancer; Life Sciences & Biomedicine; combined therapy; Oncology; targeting strategy
• Research Categories: Engineering, Biomedical; Health Sciences, Oncology

Abstract

A broad array of molecular and cellular events is associated with developing resistance to treatment, 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 throughout evolution, 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-specific targeting of mitochondrial functions may have significant unwarranted effects on normal cell growth and survival. Therefore, treatments conjugated with other anticancer therapy are needed to precisely target specific mitochondrial proteins involved in tumor progression and the acquisition of treatment resistance.