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Celecoxib decreases expression of the adhesion molecules ICAM-1 and VCAM-1 in a colon cancer cell line (HT29)

M Gallicchio1, A C Rosa, C Dianzani

  • 1Department of Anatomy, Pharmacology and Forensic Medicine, University of Turin, Torino, Italy. margherita.gallicchio@unito.it

British Journal of Pharmacology
|December 18, 2007
PubMed
Abstract

Insights

Celecoxib reduces ICAM-1 and VCAM-1 expression in colon cancer cells, impacting cell adhesion. This occurs independently of COX-2, by inhibiting p38 and JNK pathways and promoting apoptosis.

Area of Science:

  • Molecular biology
  • Cancer research
  • Pharmacology

Background:

  • Intercellular adhesion molecules (ICAM-1, VCAM-1) play roles in cancer progression.
  • Selective cyclooxygenase-2 (COX-2) inhibitors, like celecoxib, are used in cancer treatment.
  • Understanding celecoxib's effects on adhesion molecules is crucial for cancer therapy.

Purpose of the Study:

  • To investigate celecoxib's effect on ICAM-1 and VCAM-1 expression in HT29 colon cancer cells.
  • To explore the role of mitogen-activated protein kinases (MAPKs) in celecoxib's action.
  • To assess celecoxib's impact on HT29 cell adhesion and apoptosis.

Main Methods:

  • Celecoxib treatment of HT29 cells to measure ICAM-1 and VCAM-1 protein and mRNA levels.
  • Use of specific MAPK inhibitors (SB202190, SP600125) to assess pathway involvement.
  • Evaluation of HT29 cell adhesion to coated surfaces and apoptosis markers (Bax, BID, Bcl-2).

Main Results:

  • Celecoxib dose- and time-dependently downregulated ICAM-1 and VCAM-1 expression.
  • Celecoxib inhibited p38 and JNK (p55) MAPK activation, but not p46 JNK or p42/44 MAPK.
  • Inhibition of p38 and JNK pathways mimicked celecoxib's effect on ICAM-1/VCAM-1 and cell adhesion; celecoxib induced apoptosis.

Conclusions:

  • Celecoxib downregulates ICAM-1 and VCAM-1 in HT29 cells via a COX-2 independent mechanism.
  • The effect involves the inhibition of p38 and p55 JNK MAPKs, influencing cell adhesion.
  • Celecoxib activates a pro-apoptotic pathway, suggesting potential therapeutic applications.

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