heterogeneous gene expression changes in colorectal cancer cells share the wnt pathway in response to growth suppression by aphs-mediated cox-2 inhibition

Clicks: 166
ID: 173176
2008
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Steady

Ranked #21 of 61 articles by views in letters in applied microbiology

Most read Least read

Bar heights use a square-root scale.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Abstract
Bostjan Humar1, Les McNoe1, Anita Dunbier1, Rosemary Heathcott1, Antony W Braithwaite2, Anthony E Reeve11Cancer Genetics Laboratory, Department of Biochemistry; University of Otago, Dunedin, Aotearoa New Zealand; 2Children's Medical Research Institute, Wintworthbill, NSW, AustraliaAbstract: Cyclooxygenase-2 (COX-2), the prostaglandin (PG)-synthesizing enzyme overexpressed in colorectal cancer (CRC), has pleiotropic, cancer-promoting effects. COX-2inhibitors (CIBs) interfere with many cancer-associated processes and show promising antineoplastic activity, however, a common mechanism of CIB action has not yet been established. We therefore investigated by microarray the global response towards the CIB APHS at a dose significantly inhibiting the growth of three COX-2-positive CRC but not of two COX-2-negative cell lines. None of the genes significantly (p = 0.005) affected by APHS were common to all three cell lines and 83% of the altered pathways were cell line-specific. Quantitative polymerase chain reaction (QPCR) on selected pathways confirmed cell line-specific expression alterations induced by APHS. A low stringency data analysis approach using BRB array tools coupled with QPCR, however, identified small expression changes shared by all COX-2-positive cell lines in genes related to the WNT pathway, the key driver of colonic carcinogenesis. Our data indicates a substantial cell line-specificity of APHS-induced expression alterations in CRC cells and helps to explain the divergent effects reported for CIBs. Further, the shared inhibition of the WNT pathway by APHS suggests one potential common mechanism behind the antineoplastic effects of COX-2 inhibition.Keywords: antineoplastic drugs, cell lines, colon cancer, COX-2 inhibitors, DNA arrays, WNT factors
Reference Key
humar2008biologicsheterogeneous Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Bostjan Humar;Les McNoe;Anita Dunbier;Rosemary Heathcott;Antony W Braithwaite;Anthony E Reeve
Journal letters in applied microbiology
Year 2008
DOI
DOI not found
URL
Keywords

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

No comments yet. Be the first to comment on this article.