Related Experiment Video
Updated: Aug 14, 2026

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
Changes in gene expression contribute to cancer prevention by COX inhibitors
Seung Joon Baek1, Thomas E Eling
1University of Tennessee, Department of Pathobiology, College of Veterinary Medicine Knoxville, TN 37996, USA.
Abstract:
Non-steroidal anti-inflammatory drugs (NSAIDs) are used primarily for the treatment of inflammatory diseases. However, certain NSAIDs also have a chemopreventive effect on the development of human colorectal and other cancers. NSAIDs inhibit cyclooxygenase-1 (COX-1) and/or cyclooxygenase-2 (COX-2) activity and considerable evidence supports a role for prostaglandins in cancer development. However, the chemopreventive effect of NSAIDs on colorectal and other cancers appears also to be partially independent of COX activity. COX inhibitors also alter the expression of a number of genes that influence cancer development. One such gene is NAG-1 (NSAID-Activated Gene), a critical gene regulated by a number of COX inhibitors and chemopreventive chemicals. Therefore, this article will discuss the evidence supporting the conclusion that the chemo-preventive activity of COX inhibitors is mediated, in part, by altered gene expression with an emphasis on NAG-1 studies. This review may also provide new insights into how chemicals and environmental factors influence cancer development. In view of the cardiovascular and gastrointestinal toxic side effects of COX-2 inhibitors and non-selective COX inhibitors, respectively, the results presented here may provide the basis for the development of a new family of anti-tumorigenic compounds acting independent of COX inhibition.
Insights
Certain non-steroidal anti-inflammatory drugs (NSAIDs) show cancer chemopreventive effects partly through altering gene expression, like NSAID-Activated Gene (NAG-1), independent of cyclooxygenase (COX) inhibition.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Non-steroidal anti-inflammatory drugs (NSAIDs) treat inflammation and possess chemopreventive properties against colorectal and other cancers.
- NSAIDs inhibit cyclooxygenase (COX)-1 and/or COX-2, enzymes involved in prostaglandin synthesis, which plays a role in cancer development.
- The chemopreventive effects of NSAIDs may extend beyond COX inhibition, influencing gene expression related to cancer.
Purpose of the Study:
- To review evidence suggesting that the chemopreventive activity of NSAIDs and COX inhibitors is mediated, in part, by altered gene expression.
- To emphasize the role of NSAID-Activated Gene (NAG-1) in mediating these effects.
- To explore potential new anti-tumorigenic compounds acting independently of COX inhibition.
Main Methods:
- Review of existing scientific literature on NSAIDs, COX inhibitors, gene expression, and cancer chemoprevention.
- Focus on studies investigating the regulation of NAG-1 by chemopreventive agents.
- Analysis of evidence for COX-independent mechanisms of cancer prevention.
Main Results:
- NSAIDs and COX inhibitors alter the expression of genes involved in cancer development, including NAG-1.
- NAG-1 is a critical gene regulated by various COX inhibitors and chemopreventive chemicals.
- Evidence suggests a significant role for altered gene expression, particularly NAG-1, in the chemopreventive effects of NSAIDs.
Conclusions:
- The chemopreventive efficacy of NSAIDs and COX inhibitors is partly mediated by modulating gene expression, with NAG-1 being a key player.
- These findings offer insights into how environmental factors and chemicals influence cancer development.
- The identification of COX-independent pathways may lead to the development of novel anti-tumorigenic agents with reduced side effects.
Related Concept Videos
Cancer-Critical Genes I: Proto-oncogenes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes I: Proto-oncogenes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes II: Tumor Suppressor Genes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes II: Tumor Suppressor Genes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer Prevention
Some...
Cancer Prevention
Some...