MEK Activation Suppresses CPT11-Induced Apoptosis in Rat Intestinal Epithelial Cells Through a COX-2-Dependent Mechanism View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2007-10

AUTHORS

Youhei Horikawa, Michiro Otaka, Koga Komatsu, Mario Jin, Masaru Odashima, Isao Wada, Tamotsu Matsuhashi, Reina Ohba, Jinko Oyake, Natsumi Hatakeyama, Raymond N. DuBois, Sumio Watanabe

ABSTRACT

Resistance to chemotherapeutic agents is one of the distinct features of cancer cells. We evaluate the role of activated MEK-ERK signaling in Camptotecin/irinotecan (CPT-11)-induced cell death using constitutively activated MEK1-transfected normal rat intestinal epithelial cells (IEC-caMEK cells). A CPT-11-induced inhibitory concentration of 50% was determined by WST assay. Apoptosis was evaluated by DNA staining and fragmented DNA analysis. Protein expressions were analyzed by western blotting. We also examined the role of cyclooxygenase-2 in the cell systems. IEC-caMEK cells possessed survival advantages compared to control cells. Apoptosis was remarkably suppressed in IEC-caMEK cells. Western blot analysis revealed increased expression of Bcl-2, Bcl-xL, Mcl-1, and COX-2 and decreased expression of Bak in IEC-caMEK cells. The COX-2 selective inhibitor ameliorated the antiapoptotic nature of IEC-caMEK cells. MEK activation suppressed CPT-11-induced apoptosis in IEC-caMEK cells via a COX-2- dependent mechanism. Therefore, MEK-ERK signaling may contribute to the drug-resistant nature of cancer cells. More... »

PAGES

2757-2765

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s10620-007-9798-0

DOI

http://dx.doi.org/10.1007/s10620-007-9798-0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1017330689

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/17393318


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