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Diclofenac down-regulates COX-2 induced expression of CD44 and ICAM-1 in human HT29 colorectal cancer cells

Çağatay Yilmaz1, Sadi Köksoy2,3, Tuğçe Çeker1

  • 1Department of Medical Biochemistry, Faculty of Medicine, Akdeniz University, 07070, Antalya, Turkey.

Naunyn-Schmiedeberg'S Archives of Pharmacology
|August 26, 2021
PubMed

Insights

Diclofenac (DCF), a COX-2 inhibitor, reduces colorectal cancer cell adhesion molecules CD44 and ICAM-1, while increasing apoptosis. This suggests DCF may inhibit tumor growth and metastasis in COX-2-expressing colon cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Cyclooxygenase-2 (COX-2) is implicated in human colorectal cancer development.
  • Selective COX-2 inhibitors like diclofenac (DCF) may offer therapeutic potential.
  • Understanding DCF's impact on cell adhesion and apoptosis is crucial for cancer treatment.

Purpose of the Study:

  • To investigate the effect of diclofenac on cell adhesion molecules and apoptosis in human colon adenocarcinoma cells.
  • To compare these effects in cells with varying levels of COX-2 expression.
  • To elucidate the mechanisms underlying diclofenac's anti-cancer activity.

Main Methods:

  • Utilized HT29 (COX-2 overexpressing) and HCT116 (COX-2 non-expressing) colon adenocarcinoma cell lines.
  • Assessed cell viability (MTT assay), COX-2 levels/activity, and polyunsaturated fatty acids (PUFAs).
  • Analyzed cell adhesion molecules (CD44, ICAM-1, VCAM-1, EpCAM) and apoptosis (Annexin V, caspase-3 activity) via flow cytometry and fluorometric assays.

Main Results:

  • HCT116 cells showed lower CD44 and ICAM-1 expression than HT29 cells.
  • Diclofenac downregulated PMA-induced CD44 and ICAM-1 in HT29 cells.
  • Diclofenac and PMA co-treatment significantly increased apoptosis and caspase-3 activity in colon cancer cells.

Conclusions:

  • Diclofenac reduces colorectal tumor growth and metastasis in COX-2-overexpressing cells.
  • This effect is mediated by increased apoptosis and decreased expression of CD44 and ICAM-1.
  • Diclofenac demonstrates potential as a therapeutic agent for COX-2-positive colorectal cancers.
Keywords:
AdenocarcinomaApoptosisCell adhesion moleculeColon

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