Chemotherapy Resistance: Role of Mitochondrial and Autophagic Components.

Simple Summary: Chemotherapy resistance is a common occurrence during cancer treatment that cancer researchers are attempting to understand and overcome. Mitochondria are a crucial intracellular signaling core that are becoming important determinants of numerous aspects of cancer genesis and progression, such as metabolic reprogramming, metastatic capability, and chemotherapeutic resistance. Mitophagy, or selective autophagy of mitochondria, can influence both the efficacy of tumor chemotherapy and the degree of drug resistance. Regardless of the fact that mitochondria are well-known for coordinating ATP synthesis from cellular respiration in cellular bioenergetics, little is known its mitophagy regulation in chemoresistance. Recent advancements in mitochondrial research, mitophagy regulatory mechanisms, and their implications for our understanding of chemotherapy resistance are discussed in this review. Cancer chemotherapy resistance is one of the most critical obstacles in cancer therapy. One of the well-known mechanisms of chemotherapy resistance is the change in the mitochondrial death pathways which occur when cells are under stressful situations, such as chemotherapy. Mitophagy, or mitochondrial selective autophagy, is critical for cell quality control because it can efficiently break down, remove, and recycle defective or damaged mitochondria. As cancer cells use mitophagy to rapidly sweep away damaged mitochondria in order to mediate their own drug resistance, it influences the efficacy of tumor chemotherapy as well as the degree of drug resistance. Yet despite the importance of mitochondria and mitophagy in chemotherapy resistance, little is known about the precise mechanisms involved. As a consequence, identifying potential therapeutic targets by analyzing the signal pathways that govern mitophagy has become a vital research goal. In this paper, we review recent advances in mitochondrial research, mitophagy control mechanisms, and their implications for our understanding of chemotherapy resistance. [ABSTRACT FROM AUTHOR]