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  3. Pressure Activates Colon Cancer Cell Adhesion By Inside-out Focal Adhesion Complex And Actin Cytoskeletal Signaling.
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  3. Pressure Activates Colon Cancer Cell Adhesion By Inside-out Focal Adhesion Complex And Actin Cytoskeletal Signaling.

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Pressure activates colon cancer cell adhesion by inside-out focal adhesion complex and actin cytoskeletal signaling.

Vijayalakshmi Thamilselvan1, Marc D Basson

  • 1Department of Surgery, John D. Dingell VA Medical Center, Detroit, MI 48201, USA.

Gastroenterology
|December 31, 2003

View abstract on PubMed

Summary
This summary is machine-generated.

Increased pressure, like that during surgery, may enhance colon cancer cell adhesion and metastasis. This occurs through pressure-activated focal adhesion kinase (FAK) and Src signaling pathways, which are actin-dependent.

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Area of Science:

  • Cell Biology
  • Oncology
  • Biophysics

Background:

  • Metastasis is a complex process where circulating tumor cells implant and grow.
  • Venous, lymphatic, or iatrogenic pressure may activate signals that promote malignant colonocyte adhesion.

Purpose of the Study:

  • To investigate the hypothesis that increased pressure activates signals governing malignant colonocyte adhesion.
  • To elucidate the molecular mechanisms by which pressure influences colon cancer cell adhesion.

Main Methods:

  • Primary human colon cancer cells and SW620 colonocytes were subjected to increased pressure (15 mm Hg for 30 minutes).
  • Adhesion to collagen and endothelial cells was assessed, along with integrin affinity modulation by cations.
  • Focal adhesion kinase (FAK), Src, and extracellular signal-regulated kinase (ERK) activation were analyzed using Western blotting and kinase assays.
  • Specific inhibitors (PP2, SiRNA, FRNK, PD98059, calphostin C) and actin destabilization (phalloidin) were used to probe signaling pathways.

Main Results:

  • Increased pressure stimulated colonocyte adhesion to collagen and endothelial cells.
  • Pressure enhanced SW620 binding force without altering integrin surface expression.
  • Pressure activated FAK and Src signaling pathways in SW620 cells, an effect dependent on actin.
  • Inhibition of FAK and Src, but not ERK, MEK, or PKC, prevented pressure-induced adhesion.

Conclusions:

  • Extracellular pressure can increase colon cancer cell adhesion by activating FAK and Src signaling.
  • This pressure-induced, actin-dependent mechanotransduction pathway may play a critical role in regulating metastasizing tumor cell adhesion.
  • The findings contrast with the effects of divalent cations on colon cancer cell adhesion.