Expanding perspectives on the significance of mitophagy in cancer

Abstract

Mitophagy is a selective mode of autophagy in which mitochondria are specifically targeted for degradation at the autophagolysosome. Mitophagy is activated by stresses such as hypoxia, nutrient deprivation, DNA damage, inflammation and mitochondrial membrane depolarization and plays a role in maintaining mitochondrial integrity and function. Defects in mitophagy lead to mitochondrial dysfunction that can affect metabolic reprogramming in response to stress, alter cell fate determination and differentiation, which in turn affects disease incidence and etiology, including cancer. Here, we discuss how different mitophagy adaptors and modulators, including Parkin, BNIP3, BNIP3L, p62/SQSTM1 and OPTN, are regulated in response to physiological stresses and deregulated in cancers. Additionally, we explore how these different mitophagy control pathways coordinate with each other. Finally, we review new developments in understanding how mitophagy affects stemness, cell fate determination, inflammation and DNA damage responses that are relevant to understanding the role of mitophagy in cancer.

Coptisine fromCoptis chinensisexerts diverse beneficial properties: A concise review

“…Autophagy is involved in the progression of multiple disorders including cancer and CADs. [119][120][121] To date, apart from regulating transduction of pathways such as NF-κB, MAPK and PI3K/AKT, berberine has been verified to mediate mitochondrial-induced apoptosis and protective autophagy in human breast cancer cells, 122 and it also induces autophagy and the downstream NLRP3 inflammasome activation in macrophages. 123 Moreover, berberine ameliorates CADs through triggering autophagy in both Beclin-1-dependent and…”

Two enemies, one fight: An update of oral cancer in patients with Fanconi anemia

“…In addition to their participation in DNA damage repair, other findings suggest an association between FA proteins and the selective autophagy of viruses and mitochondria . Although the mechanisms of selective autophagy are not fully comprehended, it seems to be associated with infectious diseases, cancer, and conditions related to age as a result of the production of mitochondrial reactive oxygen species, which increases intracellular oxidative stress …”

Inflammasomes and their roles in the pathogenesis of viral hepatitis and their related complications: An updated systematic review

“…Chinese herbal therapy of HCC animal models led to NLRP3 inflammasome suppression, and subsequently inhibited proliferation and metastasis of HCC [83]. It has been documented that mitophagy is a biological process to remove the dysfunctional mitochondria, which is a main cause of cancers [84]. FUN14 domain containing 1 (FUNDC1), a well-characterized mitophagy receptor, mediates mitophagy and consequently suppresses HCC induction through inhibition of inflammasome activation, including caspase-1 and IL-1β [68].…”