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Interaction of integrin-linked kinase and miniature chromosome maintenance 7-mediating integrin {alpha}7 induced cell

Yu-Chen Han1, Yan P Yu, Joel Nelson

  • 1Departments of Pathology and Urology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA.

Cancer Research
|May 13, 2010
PubMed

Insights

Integrin alpha7 (ITGA7) signaling suppresses tumor growth by inducing integrin-linked kinase (ILK) to phosphorylate miniature chromosome maintenance 7 (MCM7), inhibiting cell proliferation.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Signaling

Background:

  • Integrin alpha7 (ITGA7) mutations are linked to human cancers.
  • ITGA7 expression suppresses tumor growth and motility in prostate cancer and leiomyosarcoma.

Purpose of the Study:

  • To elucidate the molecular mechanism by which ITGA7 exerts its tumor-suppressive effects.
  • To investigate the interaction between ITGA7, integrin-linked kinase (ILK), and miniature chromosome maintenance 7 (MCM7).

Main Methods:

  • Investigated the binding interaction between ILK and MCM7 using a identified 58-amino acid ILK binding motif.
  • Analyzed ITGA7-induced MCM7 phosphorylation in cell lines with and without ILK or its dominant-negative mutant (ANK).
  • Assessed the effect of MCM7 phosphorylation on MCM7 chromatin association and cell growth, including experiments with an ILK-non-binding MCM7 mutant.

Main Results:

  • ITGA7 expression induces MCM7 phosphorylation, dependent on ILK binding and activity.
  • MCM7 phosphorylation by ILK reduces MCM7 chromatin association and inhibits cell proliferation.
  • A mutant MCM7 that cannot bind ILK abrogates ITGA7's tumor-suppressive effects.

Conclusions:

  • The interaction between ILK and MCM7, leading to MCM7 phosphorylation, is a critical event in the ITGA7 signaling pathway.
  • This pathway plays a significant role in ITGA7-mediated tumor suppression.
  • Targeting the ILK-MCM7 interaction could offer novel therapeutic strategies for ITGA7-related malignancies.

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