Prostaglandins and the colon cancer connection

Trends Mol Med. 2006 Jun;12(6):240-4. doi: 10.1016/j.molmed.2006.04.006. Epub 2006 May 2.

Abstract

Colorectal cancer is a leading cause of cancer-related deaths throughout the world. Non-steroidal anti-inflammatory drugs (NSAIDs) are among the few agents that are known to inhibit colorectal tumorigenesis. The mechanisms that underlie this effect are poorly understood. Two recent studies have provided some significant insight. Castellone and colleagues showed that prostaglandin E2 modulates the beta-catenin signaling axis, a key pathway for colorectal tumorigenesis. Holla and colleagues showed that prostaglandin E2 might act via a nuclear receptor. These findings shed light on the mechanisms that underlie prostaglandin action, and provide a molecular framework for developing future treatments for colorectal cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenomatous Polyposis Coli Protein / metabolism
  • Animals
  • Antineoplastic Agents / pharmacology*
  • Antineoplastic Agents / therapeutic use
  • Axin Protein
  • Cell Transformation, Neoplastic / drug effects*
  • Cell Transformation, Neoplastic / genetics
  • Cell Transformation, Neoplastic / metabolism
  • Colonic Neoplasms / drug therapy
  • Colonic Neoplasms / enzymology*
  • Colonic Neoplasms / genetics
  • Cyclooxygenase 2 / metabolism*
  • Cyclooxygenase 2 Inhibitors / pharmacology*
  • Cyclooxygenase 2 Inhibitors / therapeutic use
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism
  • Dinoprostone / metabolism*
  • Gene Expression Regulation, Neoplastic*
  • Glycogen Synthase Kinase 3 / metabolism
  • Glycogen Synthase Kinase 3 beta
  • Humans
  • Membrane Proteins / metabolism*
  • Nuclear Receptor Subfamily 4, Group A, Member 2
  • PPAR gamma / genetics
  • PPAR gamma / metabolism
  • Randomized Controlled Trials as Topic
  • Receptors, Prostaglandin E / metabolism
  • Repressor Proteins / metabolism
  • Signal Transduction
  • Transcription Factors / genetics
  • Transcription Factors / metabolism
  • beta Catenin / metabolism

Substances

  • Adenomatous Polyposis Coli Protein
  • Antineoplastic Agents
  • Axin Protein
  • Cyclooxygenase 2 Inhibitors
  • DNA-Binding Proteins
  • Membrane Proteins
  • NR4A2 protein, human
  • Nuclear Receptor Subfamily 4, Group A, Member 2
  • PPAR gamma
  • Receptors, Prostaglandin E
  • Repressor Proteins
  • Transcription Factors
  • beta Catenin
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • Glycogen Synthase Kinase 3 beta
  • Glycogen Synthase Kinase 3
  • Dinoprostone