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Mitochondrial dysfunction in breast cancer

Authors Riar AK, Kenny T, Takabatake Y, Papa L, Germain D

Received 22 April 2015

Accepted for publication 9 July 2015

Published 11 September 2015 Volume 2015:6 Pages 137—145


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 5

Editor who approved publication: Professor Zvi Kelman

Amanjot Kaur Riar,* Timothy C Kenny,* Yukie Takabatake,* Luena Papa, Doris Germain

Division of Hematology/Oncology, Icahn School of Medicine at Mount Sinai, Tisch Cancer Institute, New York, NY, USA

*These authors have contributed equally to this work

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 (UPRmt) and regulate the expression of one or more genes involved in these "mito-protective" mechanisms, the UPRmt is a prime candidate to coordinate the maintenance of the integrity of the mitochondria under oxidative stress conditions.

Keywords: mitochondrial unfolded protein response (UPRmt), mitochondrial DNA, SOD2, reactive oxygen species, breast cancer, mitomiRs, mitochondrial protein quality controls

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