Mitochondrial dysfunction in breast cancer

Abstract

Abstract:The reprogramming of the mitochondria of cancer cells is essential for their growth. However, such reprogramming leads to the increased formation of reactive oxygen species, which can lead to damage to the organelle. This review summarizes the mechanisms that protect the mitochondrial network against oxidative stress. Further, since several transcription factors have now been linked to the mitochondrial unfolded protein response (UPR mt ) and regulate the expression of one or more genes involved in these "mito-protective" mechanisms, the UPR mt is a prime candidate to coordinate the maintenance of the integrity of the mitochondria under oxidative stress conditions.

Potential Association of Mitochondrial Haplogroups and A8860G Mutation with Breast Cancer Risk

“…It is well known that (mtDNA) has a mutation rate several times higher than nuclear DNA [15], due to its limited repair mechanisms, lack of protective histones and its close proximity to the electron transport chain, which continuously generates free radicals [16]; in addition, mtDNA is organized in an economic pattern with its genes lacking introns [17]. It was in 1956, when Otto Warburg observed that cancers ferment glucose in the presence of oxygen, proposing that abnormalities in mitochondrial respiration may be responsible for cancer production [16, 18, and 19]. Now it’s well-established that changes in the biochemical processes that accompany the process of carcinogenesis as the aerobic glycolesis do not impair mitochondrial function but are rather essential for cancer cell viability [15].…”