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Insulin promotes cell migration by regulating PSA-NCAM.

Hector J Monzo1, Natacha Coppieters1, Thomas I H Park2

  • 1Centre for Brain Research, Faculty of Medical and Health Sciences, The University of Auckland, Private Bag, 92019, Auckland, New Zealand; Department of Anatomy and Medical Imaging, Faculty of Medical and Health Sciences, The University of Auckland, Private Bag, 92019, Auckland, New Zealand.

Experimental Cell Research
|March 26, 2017
PubMed
Summary
This summary is machine-generated.

Insulin promotes cell migration by regulating polysialic acid-neural cell adhesion molecule (PSA-NCAM) turnover. This involves insulin enhancing focal adhesion kinase (FAK) phosphorylation, which affects αv-integrin/PSA-NCAM clusters and cell movement.

Keywords:
ECMInsulinIntegrinMigrationP-FAKPSA-NCAM

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Cell surface polysialic acid (PSA) on neural cell adhesion molecule (NCAM) modulates cellular interactions with the extracellular environment.
  • PSA-NCAM is implicated in differentiation, plasticity, and migration, and is elevated in Alzheimer's disease and metastatic cancers.
  • Previous studies showed insulin increases cell surface PSA by inhibiting PSA-NCAM endocytosis.

Purpose of the Study:

  • To elucidate the mechanism of insulin-dependent inhibition of PSA-NCAM turnover impacting cell migration.
  • To investigate the role of focal adhesion kinase (FAK) and αv-integrin in this process.

Main Methods:

  • Investigated insulin's effect on PSA-NCAM turnover and cell migration.
  • Analyzed the phosphorylation of focal adhesion kinase (FAK).
  • Examined the interaction between αv-integrin and PSA-NCAM using knockdown and co-labeling studies with Rab5.

Main Results:

  • Insulin enhanced FAK phosphorylation, leading to dissociation of αv-integrin/PSA-NCAM clusters and promoting cell migration.
  • αv-integrin knockdown inhibited PSA-NCAM endocytosis, and αv-integrin/PSA-NCAM clusters co-localized with Rab5, indicating its role in internalization.
  • Inhibition of phosphorylated FAK (p-FAK) disrupted αv-integrin/PSA-NCAM clusters, reduced cell surface PSA, and impaired cell migration.

Conclusions:

  • A functional link exists between insulin/p-FAK-regulated PSA-NCAM turnover and cell migration through the extracellular matrix.
  • Identified a novel mechanism for insulin-stimulated cell migration involving PSA-NCAM regulation.