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The term Mitophagy has been newly concerned in reforming metabolic landscape inside cancerous cells in addition to
interface between malignant cells as well as other major constituents of tumor microenvironment. Several profoundly interrelated
systems, comprising mitochondrial dynamics and mitophagy, function in mammalian cells as vital mitochondrial regulator process, and
their consequence in neoplastic development has newly illuminated clinically. In specific instance of cancer cells, mitochondrialprotected metabolic paths are revamped to meet expanded bioenergetics along with biosynthetic necessities of malignant cells in addition
to deal with oxidative stress. It is an exhausting task to foresee the role that mitophagy has on malignant growth cells since it relies upon
various elements like cancer variability, malignant growth phase, genetic background and harmony between cell demand and
accessibility. As per condition, mitophagy may have a double role as cancer suppressor for example Atg5 (autophagy related 5) or Atg7
(autophagy related 7) or execute promoter like function for instance FUNDC1 (FUN14 domain-containing protein 1), BNIP3
(BCL2/adenovirus E1B 19-kDa-interacting protein 3), PINK1 (PTEN-instigated kinase 1) etc. Tumor suppressive function of Parkin (E3
ubiquitin ligase) is likewise distinguished in mammary gland carcinoma where obstruction of mitophagy impacts tumor progression. In
pancreatic cancer cells and in hepatocellular carcinoma hypermethylation of the BNIP3, promoter occurs that prevent HIF-1 (HypoxiaInducible Factor 1) binding besides ensuing initiation of mitophagy. Since the double role mitophagy has in malignant growth relying
upon various circumstances and cell varieties, a range of studies have been going on mitophagy and its role in cancer progression and
development is opening up a new paradigm with immense clinical importance.