Tuesday, 28 October 2014

Mitochondrial ROS in cancer: initiators, amplifiers or an Achilles’ heel?

Mitochondrial ROS in cancer: initiators, amplifiers or an Achilles’ heel?

Reactive oxygen species (ROS) are typically generated by the leak of electrons from the electron transport chain (ETC) in mitochondria: the powerhouse of the cell. The function of ROS in both normal and pathological circumstances is subtle, as highlighted by this review. ROS are thought to damage mitochondrial DNA, which may result in the ETC becoming more leaky, to generate more ROS. ROS can switch on a variety of pro-survival signals such as HIF, MAPK-ERK and AMPK in cancer, as well as causing nuclear DNA-damage to increase the chances of oncogenic mutations. However, through controversial mechanisms, ROS can also act as death inducers in cancer, perhaps by spurring on apoptotic signalling. The authors argue that ROS are in fact the initiators, amplifiers and the Achilles' heel of cancer.

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