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Review
. 2019 Mar;76(5):827-835.
doi: 10.1007/s00018-018-2961-2. Epub 2018 Nov 10.

Mitochondrial dynamics and metastasis

Dario C Altieri  1
Affiliations
Review

Mitochondrial dynamics and metastasis

Dario C Altieri. Cell Mol Life Sci. 2019 Mar.

Abstract

Changes in cellular metabolism are now a recognized hallmark of cancer. Although this process is ripe with therapeutic potential in the clinic, its complexity and extraordinary plasticity have systematically defied dogmas and oversimplifications. Perhaps, best exemplifying this intricacy is the role of mitochondria in cancer, which in just a few years has gone from largely unnoticed to pivotal disease driver. The underlying mechanisms are only beginning to emerge. However, there is now clear evidence linking the dynamic nature of mitochondria to the machinery of tumor cell motility and metastatic spreading. These studies may open fresh therapeutic options for patients with disseminated cancer, currently an incurable and mostly lethal condition.

Keywords: Cancer; Dynamics; Metastasis; Mitochondria; Trafficking; Tumor cell invasion.

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Conflict of interest statement

The author declares that no conflict of interest exists.

Figures

Fig. 1
Fig. 1
Cellular machinery of mitochondrial dynamics. Schematic diagrams representing modulation of mitochondrial fusion, quality control/mitophagy, fission, and subcellular trafficking are shown
Fig. 2
Fig. 2
Subcellular mitochondrial trafficking in tumor cells. Glioblastoma LN229 cells were transfected with control vector or FLAG-syntaphilin cDNA and analyzed for subcellular mitochondrial localization by confocal laser microscopy. 3D rendering of representative images is shown. The individual labeling for FLAG-syntaphilin (SNPH), nuclei, mitochondria, or actin is indicated. Reproduced from Caino et al. [78]
Fig. 3
Fig. 3
Dual function of syntaphilin (SNPH) in cancer. In the presence of nutrients and oxygen (O2) in a favorable microenvironment (a), high SNPH levels at the inner and outer mitochondrial membranes support tumor cell proliferation via oxidative phosphorylation and reduced ROS, while preventing mitochondrial trafficking to the cortical cytoskeleton and tumor cell movements. In contrast, low nutrients and oxygen (O2) in an unfavorable microenvironment (b) decrease SNPH levels resulting in reduced ATP production, greater ROS generation, and released inhibition of mitochondrial trafficking, triggering decreased tumor cell proliferation but heightened tumor cell motility and invasion
See this image and copyright information in PMC

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