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Related Concept Videos

Activation of Integrins01:15

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Integrins bind ligands and transmit information from outside the cell to inside or vice-versa through an "outside-in signaling" or "inside-out signaling."
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Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
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Related Experiment Video

Updated: Apr 19, 2026

Examining the Dynamics of Cellular Adhesion and Spreading of Epithelial Cells on Fibronectin During Oxidative Stress
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OXPHOS dysfunction regulates integrin-β1 modifications and enhances cell motility and migration.

Joana B Nunes1, Joana Peixoto2, Paula Soares1

  • 1Institute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Porto, Portugal, Medical Faculty and.

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Mitochondrial DNA (mtDNA) mutations causing oxidative phosphorylation (OXPHOS) dysfunction enhance cancer cell migration and invasion. This dysfunction increases tumor growth and metastasis, potentially via mitochondria-extracellular matrix interactions.

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Area of Science:

  • Cellular Biology
  • Cancer Research
  • Mitochondrial Biology

Background:

  • Mitochondria are vital for cellular metabolism.
  • Mitochondrial oxidative phosphorylation (OXPHOS) dysfunction is linked to cancer progression, including migration, invasion, metastasis, and apoptosis resistance.

Purpose of the Study:

  • To investigate the effects of OXPHOS dysfunction in cancer cells.
  • To identify molecular players involved in OXPHOS dysfunction-driven cancer cell behaviors.

Main Methods:

  • Generated cybrid cell lines with wild-type (WT) or mutant mitochondrial DNA (mtDNA) carrying the A3243T mutation (tRNAmut cybrids).
  • Assessed cellular metabolism (oxygen consumption, glucose consumption, lactate production).
  • Evaluated cell motility, migration, integrin-β1 N-glycosylation, membrane-bound integrin-β1 levels, fibronectin binding, in vitro growth, and in vivo tumor formation/metastasis in nude mice.

Main Results:

  • tRNAmut cybrids showed reduced oxygen consumption and increased glucose consumption/lactate production compared to WT cybrids.
  • tRNAmut cybrids exhibited enhanced motility and migration, linked to altered integrin-β1 N-glycosylation (increased β-1,6-GlcNAc branching), higher membrane-bound integrin-β1, and increased fibronectin binding.
  • While tRNAmut cybrids had lower in vitro growth rates, they formed larger tumors and showed higher metastatic potential in vivo.

Conclusions:

  • mtDNA-driven OXPHOS dysfunction correlates with increased cancer cell motility and migration.
  • The mechanism may involve crosstalk between cancer cell mitochondria and the extracellular matrix.
  • OXPHOS dysfunction promotes aggressive cancer phenotypes, including enhanced tumor growth and metastasis.