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Somatostatin inhibits colon cancer cell growth through cyclooxygenase-2 downregulation

R Colucci1, C Blandizzi, N Ghisu

  • 1Department of Internal Medicine, University of Pisa, Pisa, Italy.

British Journal of Pharmacology
|July 1, 2008
PubMed
Abstract

Insights

Somatostatin-14 inhibits colon cancer cell growth by reducing cyclooxygenase-2 (COX-2) and prostaglandin E(2) (PGE(2)) production through sst(3) or sst(5) receptor activation. These findings offer potential therapeutic strategies targeting the COX-2 pathway.

Area of Science:

  • Gastroenterology
  • Oncology
  • Molecular Biology

Background:

  • Cyclooxygenase-2 (COX-2) promotes colon cancer cell proliferation through prostaglandin E(2) (PGE(2)) production.
  • COX-2 is a validated therapeutic target in colorectal neoplasms.

Purpose of the Study:

  • To investigate the effects of somatostatin-14 on COX-2 expression, PGE(2) production, and proliferation in human colon cancer cell lines.
  • To elucidate the specific somatostatin receptor subtypes involved in these processes.

Main Methods:

  • Utilized human colon adenocarcinoma cell lines (Caco-2, HT-29, HCT116).
  • Assessed cell growth, DNA synthesis, and PGE(2) production.
  • Employed COX-2 mRNA silencing, RT-PCR, and Western blotting to analyze receptor expression and signaling pathways (ERK, Akt).

Main Results:

  • Somatostatin-14 inhibited COX-2 expression, PGE(2) production, DNA synthesis, and growth in Caco-2 cells, effects blocked by an sst(3) antagonist.
  • HT-29 cells, stimulated with gastrin-17, showed increased COX-2 expression, PGE(2) production, DNA synthesis, and growth, all counteracted by somatostatin-14.
  • Somatostatin-14's inhibitory effects on COX-2, PGE(2), and DNA synthesis in HT-29 cells were blocked by an sst(5) antagonist.

Conclusions:

  • Somatostatin-14 exerts anti-proliferative effects in colon cancer cells by suppressing COX-2 expression and function.
  • These actions are mediated via the activation of either sst(3) or sst(5) receptors.
  • Findings support the development of therapeutic strategies targeting the COX-2 pathway and somatostatin receptors for colorectal cancer treatment.

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