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Elevated c-Src is linked to altered cell-matrix adhesion rather than proliferation in KM12C human colorectal cancer

R J Jones1, E Avizienyte, A W Wyke

  • 1Beatson Institute for Cancer Research, Cancer Research UK Beatson Laboratories, Garscube Estate, Switchback Road, Bearsden, Glasgow G61 1BD, Scotland, UK.

British Journal of Cancer
|October 29, 2002
PubMed

Insights

Elevated cellular Src ()$ in colon cancer cells enhances cell-matrix adhesion, not proliferation. This suggests Src kinase activity influences cancer cell attachment and motility.

Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Biology

Background:

  • Elevated expression/activity of c-Src ()$ is linked to human colon cancer development.
  • Src family kinases regulate cell growth and integrin adhesions, but their role in epithelial cancer cells is unclear.

Purpose of the Study:

  • To investigate if elevated cellular Src ()$ alters cell proliferation and/or cell-matrix adhesion in colorectal cancer metastasis models.

Main Methods:

  • Utilized the Fidler model of colorectal metastasis.
  • Assessed cell proliferation in vitro and in vivo (subcutaneous tumors).
  • Evaluated cell-matrix adhesion, specifically to fibronectin.
  • Used Src inhibitors and enforced Src elevation in non-metastatic cells.

Main Results:

  • Elevated Src ()$ correlated with metastasis but not enhanced proliferation (in vitro or in vivo).
  • Elevated Src ()$ was associated with enhanced attachment to extracellular matrix.
  • Src inhibition suppressed fibronectin adhesion; enforced Src elevation stimulated fibronectin adhesion and adhesion complex assembly without affecting cell growth.

Conclusions:

  • Elevated Src ()$ in colon cancer cells modulates integrin-dependent cell-matrix attachment and adhesion structures.
  • This modulation may influence cancer cell motility and integrin-dependent cellular responses.

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