COX-2 gene expression in colon cancer tissue related to regulating factors and promoter methylation status
2011

COX-2 Gene Expression in Colon Cancer and Its Regulation

Sample size: 48 publication 10 minutes Evidence: moderate

Author Information

Author(s): Asting Annika Gustafsson, Carén Helena, Andersson Marianne, Lönnroth Christina, Lagerstedt Kristina, Lundholm Kent

Primary Institution: Sahlgrenska Academy, Sahlgrenska University Hospital, Gothenburg, Sweden

Hypothesis

The study aims to define external cell signaling and transcription factors relating to high COX-2 expression in colon cancer tissue.

Conclusion

Transcription and external cell signaling factors are altered in relation to COX-2 expression in colon cancer tissue, while DNA methylation of the COX-2 promoter region is not a significant factor.

Supporting Evidence

  • High COX-2 expression in tumors was associated with significant changes in gene expression compared to normal colon tissue.
  • Numerous genes were found to be up-regulated in tumors with high COX-2 expression.
  • IL1β, IL6, and iNOS transcripts were up-regulated in relation to COX-2 expression.
  • DNA methylation of the COX-2 promoter region was not observed in the majority of tumor specimens.

Takeaway

This study looked at how certain signals in the body affect a gene called COX-2 in colon cancer, finding that these signals change a lot but that a specific type of gene change (methylation) doesn't seem to matter.

Methodology

Tumor and normal colon tissue were collected from 48 patients, and COX-2 expression was quantified using microarray analyses and PCR.

Potential Biases

Potential selection bias as only patients undergoing surgery were included.

Limitations

The study only included patients who underwent surgery and did not account for those who received neoadjuvant treatments.

Participant Demographics

54% males and 46% females, mean age 72.5 years.

Statistical Information

P-Value

0.002

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1186/1471-2407-11-238

Want to read the original?

Access the complete publication on the publisher's website

View Original Publication