Mechanisms for the prevention of gastrointestinal cancer: The role of prostaglandin E2

Michael G. Backlund; Jason R. Mann; Raymond N. DuBois

doi:10.1159/000086629

Mechanisms for the prevention of gastrointestinal cancer: The role of prostaglandin E₂

Michael G. Backlund, Jason R. Mann, Raymond N. DuBois

Research output: Contribution to journal › Article › peer-review

89 Scopus citations

Abstract

Carcinoma of the colon or rectum represents one of the most common malignancies worldwide with a higher prevalence in industrialized regions. Epidemiologic studies of individuals taking non-steroidal anti-inflammatory drugs (NSAIDs) have shown a significant reduction in colorectal cancer (CRC) mortality compared to those individuals not receiving these agents. NSAIDs inhibit the enzymatic activity of both isoforms of cyclooxygenase (COX-1 and COX-2), while COX-2-selective inhibitors have shown some efficacy in reducing polyp formation. COX-2-derived bioactive lipids, including the primary prostaglandin (PG) generated in colorectal tumors, PGE₂, are known to stimulate cell migration, proliferation and tumor-associated neovascularization while inhibiting cell death. Here we briefly review the role of NSAIDs in preventing CRC, as well as the proposed mechanism by which a COX-2-derived PG, PGE₂, promotes colon cancer.

Original language	English (US)
Pages (from-to)	28-32
Number of pages	5
Journal	Oncology
Volume	69
Issue number	SUPPL. 1
DOIs	https://doi.org/10.1159/000086629
State	Published - 2005
Externally published	Yes

Keywords

15-Hydroxyprostaglandin dehydrogenase
Colorectal cancer
Cyclooxygenase 2
Prostaglandin E

ASJC Scopus subject areas

Oncology
Cancer Research

Access to Document

10.1159/000086629

Cite this

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title = "Mechanisms for the prevention of gastrointestinal cancer: The role of prostaglandin E2",

abstract = "Carcinoma of the colon or rectum represents one of the most common malignancies worldwide with a higher prevalence in industrialized regions. Epidemiologic studies of individuals taking non-steroidal anti-inflammatory drugs (NSAIDs) have shown a significant reduction in colorectal cancer (CRC) mortality compared to those individuals not receiving these agents. NSAIDs inhibit the enzymatic activity of both isoforms of cyclooxygenase (COX-1 and COX-2), while COX-2-selective inhibitors have shown some efficacy in reducing polyp formation. COX-2-derived bioactive lipids, including the primary prostaglandin (PG) generated in colorectal tumors, PGE2, are known to stimulate cell migration, proliferation and tumor-associated neovascularization while inhibiting cell death. Here we briefly review the role of NSAIDs in preventing CRC, as well as the proposed mechanism by which a COX-2-derived PG, PGE2, promotes colon cancer.",

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