Abstract
Mitochondria are dynamic organelles that alter their organization in response to a variety of cellular cues. Mitochondria are central in many biologic processes, such as cellular bioenergetics and apoptosis, and mitochondrial network morphology can contribute to those physiologic processes. Some of the biologic processes that are in part governed by mitochondria are also commonly deregulated in cancers. Furthermore, patient tumor samples from a variety of cancers have revealed that mitochondrial dynamics machinery may be deregulated in tumors. In this review, we will discuss how commonly mutated oncogenes and their downstream effector pathways regulate the mitochondrial dynamics machinery to promote changes in mitochondrial morphology as well as the physiologic consequences of altered mitochondrial morphology for tumorigenic growth.
Highlights
Mitochondria are double-membrane-bound organelles that are central to a variety of cellular physiological processes, such as the regulation of bioenergetics, the maintenance of cellular oxidation-reduction status, and the execution of apoptosis
In contrast to the data indicating that phosphoinositide 3-kinase (PI3K)/Akt activity promotes mitochondrial fragmentation, Caino et al showed that reactivation of Akt and mammalian target of rapamycin (mTOR) following PI3K inhibition led to increased mitochondrial fusion [84]
This study found that mitofusin 2 (Mfn2) binds to rapamycin-insensitive companion of mTOR (RICTOR), a member of the mammalian target of rapamycin complex 2 (mTORC2) complex, and is required for the inhibition of mTORC2 signaling and Akt activation
Summary
Mitochondria are double-membrane-bound organelles that are central to a variety of cellular physiological processes, such as the regulation of bioenergetics, the maintenance of cellular oxidation-reduction (redox) status, and the execution of apoptosis. The mitochondrial network can exist along a spectrum of morphologies from a highly interconnected, elongated network to a highly fragmented, punctate morphology. The mitochondrial network constantly undergoes mitochondrial fusion and fission events, and the relative balance of these activities results in a mixture of interconnected, intermediate, or fragmented morphology. Different cellular cues and signals converge upon the regulators of mitochondrial dynamics to alter mitochondrial morphology, and the morphological state confers properties appropriate for the conditions. Elongated mitochondrial morphology allows for complementation of damaged mitochondrial components under conditions of stress, while mitochondrial fragmentation allows for easier transport of mitochondria along the cytoskeleton to areas of high energy demand [1,2]. We will review recent studies that demonstrate how common oncogenic signaling pathways converge upon mitochondrial dynamics regulators and contribute to the tumorigenic phenotypes.
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