Gene interactions and pathways from curated databases and text-mining
Eur J Cancer 2006, PMID: 16914308

5-aminosalicylic acid enhances anchorage-independent colorectal cancer cell death.

Fina, Daniele; Franchi, Luigi; Caruso, Roberta; Peluso, Ilaria; Naccari, Gian Carlo; Bellinvia, Salvatore; Testi, Roberto; Pallone, Francesco; Monteleone, Giovanni

Resistance to anoikis, the cell death triggered by the loss of anchorage to the substratum, is an essential prerequisite in the proliferation and diffusion of colorectal cancer (CRC) cells. We examined whether 5-aminosalicylic acid (5-ASA), a drug that seems to reduce the risk of colitis-associated CRC, enhances CRC cell anoikis. To this end, Colo205 cells were treated with 5-ASA in the presence or absence of inhibitors of caspases (zVAD-fmk) and reactive oxygen species (ROS). We demonstrate that 5-ASA enhances Colo205 cell death. Although 5-ASA induces dissipation of mitochondrial transmembrane potential and caspase-3 activation, zVAD-fmk does not completely prevent the 5-ASA-induced cell death. 5-ASA also enhances the synthesis of ROS. However, inhibitors of ROS reduce the fraction of 5-ASA-induced Colo205 cell death but do not confer protection. In contrast, the 5-ASA-mediated Colo205 cell death is preventable by Bcl-2 over-expression. These data suggest a mechanism by which 5-ASA interferes with colon carcinogenesis.

Diseases/Pathways annotated by Medline MESH: Colorectal Neoplasms
Document information provided by NCBI PubMed

Text Mining Data

caspase-3 → 5-ASA: " Although 5-ASA induces dissipation of mitochondrial transmembrane potential and caspase-3 activation, zVAD-fmk does not completely prevent the 5-ASA induced cell death "

Manually curated Databases

No curated data.