Mitophagy in tumor: foe or friend？

Mitophagy is a specific type of autophagy and a selective form of autophagy on a larger scale. It selectively eliminates damaged, misfolded, and surplus mitochondria, particularly those that are cytotoxic, by using autophagic lysosomes. This process is crucial for maintaining a balance of both the quality and quantity of mitochondria, which is necessary for normal cell function and tissue development. However, in certain abnormal situations, such as nutritional deficiencies and hypoxia, the function of mitophagy becomes impaired. This leads to a failure to clear damaged mitochondria in a timely manner, resulting in the production of a large number of reactive oxygen species. These reactive oxygen species further contribute to an inflammatory response and the release of factors that induce apoptosis. Moreover, abnormal mitophagy can also cause mitochondrial dysfunction, disrupt metabolic reprogramming during stress responses, alter cell fate decisions and differentiation, and consequently impact the development and progression of diseases, including cancer. Therefore, mitophagy plays a crucial role in controlling the quality of cancer cells, making it imperative to study its function and impact. Numerous proteins and molecules are involved in the regulation of mitophagy, with Parkin and PTEN-induced kinase 1 (PINK1) serving as key mediators, and the hypoxia-related proteins hypoxia-inducible factor la (HIF1a) and FUN14 domain-containing 1 (FUNDC1) also playing a role. Additionally, proteins such as chromatin licensing and DNA replication factor 1 (CDT-1), insulin-like growth factor 1 (IGF-1), caveolin 1 (Cav-1), and others contribute to the regulation of mitophagy in various ways. This article aims to explore the dual role of mitophagy in tumourigenesis by examining the factors and proteins associated with mitophagy and their regulatory effects. The objective of this review is to provide a new theoretical foundation and direction for cancer treatment.