Altered mitochondrial trafficking as a novel mechanism of cancer metastasis

Cancer Rep (Hoboken). 2020 Feb;3(1):e1157. doi: 10.1002/cnr2.1157. Epub 2019 Feb 14.

Abstract

Background: Mammalian cells must constantly reprogram the distribution of mitochondria in order to meet the local demands for energy, calcium, redox balance, and other mitochondrial functions. Mitochondrial localization inside the cell is a result of a combination of movement along the microtubule tracks plus anchoring to actin filaments.

Recent findings: Recent advances show that subcellular distribution of mitochondria can regulate tumor cell growth, proliferation/motility plasticity, metastatic competence, and therapy responses in tumors. In this review, we discuss our current understanding of the mechanisms by which mitochondrial subcellular distribution is regulated in tumor cells.

Conclusions: Mitochondrial trafficking is dysregulated in tumors. Accumulation of mitochondria at the leading edge of the cell supports energy expensive processes of focal adhesion dynamics, cell membrane dynamics, migration, and invasion.

Keywords: cancer; dynein; kinesin; mitochondria; myosin; trafficking.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adenosine Triphosphate / metabolism
  • Animals
  • Cell Movement
  • Focal Adhesions
  • Humans
  • Membrane Proteins / physiology
  • Microtubules / physiology
  • Mitochondria / physiology*
  • Myosin Heavy Chains / physiology
  • Myosin Type V / physiology
  • Myosins / physiology
  • Neoplasm Invasiveness
  • Neoplasm Metastasis*
  • Nerve Tissue Proteins / physiology
  • Signal Transduction

Substances

  • Membrane Proteins
  • Myo19 protein, human
  • Nerve Tissue Proteins
  • SNPH protein, human
  • MYO5A protein, human
  • Adenosine Triphosphate
  • Myosin Type V
  • Myosin Heavy Chains
  • Myosins