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2017 ; 9
(7
): 349-351
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Parkin in cancer: Mitophagy-related/unrelated tasks
#MMPMID28321271
Eid N
; Kondo Y
World J Hepatol
2017[Mar]; 9
(7
): 349-351
PMID28321271
show ga
Dysfunctional mitochondria may produce excessive reactive oxygen species, thus
inducing DNA damage, which may be oncogenic if not repaired. As a major role of
the PINK1-Parkin pathway involves selective autophagic clearance of damaged
mitochondria via a process termed mitophagy, Parkin-mediated mitophagy may be a
tumor-suppressive mechanism. As an alternative mechanism for tumor inhibition
beyond mitophagy, Parkin has been reported to have other oncosuppressive
functions such as DNA repair, negative regulation of cell proliferation and
stimulation of p53 tumor suppressor function. The authors recently reported that
acute ethanol-induced mitophagy in hepatocytes was associated with Parkin
mitochondrial translocation and colocalization with accumulated 8-OHdG (a marker
of DNA damage and mutagenicity). This finding suggests: (1) the possibility of
Parkin-mediated repair of damaged mitochondrial DNA in hepatocytes of
ethanol-treated rats (ETRs) as an oncosuppressive mechanism; and (2) potential
induction of cytoprotective mitophagy in ETR hepatocytes if mitochondrial damage
is too severe to be repaired. Below is a summary of the various roles Parkin
plays in tumor suppression, which may or may not be related to mitophagy. A
proper understanding of the various tasks performed by Parkin in tumorigenesis
may help in cancer therapy by allowing the PINK1-Parkin pathway to be targeted.
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