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2016 ; 8
(4
): ä Nephropedia Template TP
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Mitochondrial Redox Signaling and Tumor Progression
#MMPMID27023612
Chen Y
; Zhang H
; Zhou HJ
; Ji W
; Min W
Cancers (Basel)
2016[Mar]; 8
(4
): ä PMID27023612
show ga
Cancer cell can reprogram their energy production by switching mitochondrial
oxidative phosphorylation to glycolysis. However, mitochondria play multiple
roles in cancer cells, including redox regulation, reactive oxygen species (ROS)
generation, and apoptotic signaling. Moreover, these mitochondrial roles are
integrated via multiple interconnected metabolic and redox sensitive pathways.
Interestingly, mitochondrial redox proteins biphasically regulate tumor
progression depending on cellular ROS levels. Low level of ROS functions as
signaling messengers promoting cancer cell proliferation and cancer invasion.
However, anti-cancer drug-initiated stress signaling could induce excessive ROS,
which is detrimental to cancer cells. Mitochondrial redox proteins could
scavenger basal ROS and function as "tumor suppressors" or prevent excessive ROS
to act as "tumor promoter". Paradoxically, excessive ROS often also induce DNA
mutations and/or promotes tumor metastasis at various stages of cancer
progression. Targeting redox-sensitive pathways and transcriptional factors in
the appropriate context offers great promise for cancer prevention and therapy.
However, the therapeutics should be cancer-type and stage-dependent.
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