Etodolac, a selective cyclo-oxygenase-2 inhibitor, enhances carboplatin-induced apoptosis of human tongue carcinoma cells by down-regulation of FAP-1 expression
| Autor: | Yasuro Yoshimura, Koichi Mishima, Yoshiki Nariai |
|---|---|
| Rok vydání: | 2005 |
| Předmět: |
Cancer Research
Blotting Western Protein Tyrosine Phosphatase Non-Receptor Type 13 Down-Regulation Antineoplastic Agents Apoptosis Protein tyrosine phosphatase Carboplatin chemistry.chemical_compound Tumor Cells Cultured medicine Humans Cyclooxygenase Inhibitors FADD Etodolac neoplasms biology Reverse Transcriptase Polymerase Chain Reaction business.industry Drug Synergism Neoplasm Proteins Tongue Neoplasms Squamous carcinoma Oncology chemistry Enzyme inhibitor Cell culture Immunology Carcinoma Squamous Cell Cancer research biology.protein Protein Tyrosine Phosphatases Oral Surgery Carrier Proteins business medicine.drug |
| Zdroj: | Oral Oncology. 41:77-81 |
| ISSN: | 1368-8375 |
| DOI: | 10.1016/j.oraloncology.2004.06.009 |
| Popis: | Summary The human tongue well-differentiated squamous carcinoma cell line, SCC-25, shows Fas-dependent apoptosis by treatment with carboplatin (CBDCA). FADD is markedly up-regulated by CBDCA, resulting in the induction of apoptosis. FAP-1, antiapoptotic tyrosine phosphatase, is expressed in the cytosol and blocks the transduction of the “death signal” from Fas to downstream. In this study, we show that etodolac, a selective cyclo-oxygenase-2 inhibitor, enhanced CBDCA-induced apoptosis of SCC-25, although etodolac alone did not induce the apoptosis. In combination with CBDCA, etodolac significantly decreased FAP-1 expression both at protein and mRNA levels, although etodolac by itself did not inhibit FAP-1 expression. These results indicate that etodolac, when combined with CBDCA, can enhance an action of anticancer drug through the suppression of FAP-1 expression. |
| Databáze: | OpenAIRE |
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