Abstract | PURPOSE: METHODS: RESULTS: DODC alone was able to induce apoptotic cell death but not decrease of telomerase activity in nasopharyngeal carcinoma NPC-TW01 cells. Instead, we found evidence that DODC significantly affected cellular mitochondria. DODC inhibited the uptake of another mitochondrial probe 3,3'-dihexyloxacarbocyanine iodide. By proteomic comparative analysis, we found that DODC induced the increase of prohibitin level in the mitochondria, indicating the occurrence of mitochondrial perturbation. Moreover, DODC was found to induce the levels of p53 and an 18-kDa truncated Bax on mitochondria, which in turn potentiated the release of cytochrome c for activation of caspases. CONCLUSIONS: DODC induces NPC-TW01 cell apoptosis via a mitochondrion-mediated mechanism. This paper demonstrates another cytotoxic mechanism of DODC other than inhibition of telomerase.
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Authors | Chung-Pin Li, Jen-Hsin Huang, Ai-Chi Chang, Yi-Mei Hung, Chao-Hsiung Lin, Yee Chao, Shou-Dong Lee, Jacqueline Whang-Peng, Tze-Sing Huang |
Journal | Pharmaceutical research
(Pharm Res)
Vol. 21
Issue 1
Pg. 93-100
(Jan 2004)
ISSN: 0724-8741 [Print] United States |
PMID | 14984262
(Publication Type: Comparative Study, Journal Article)
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Chemical References |
- Carbocyanines
- Ligands
- Guanosine
- 3,3'-diethyloxadicarbocyanine
- DNA
- Telomerase
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Topics |
- Apoptosis
(drug effects, physiology)
- Carbocyanines
(metabolism, pharmacology)
- Cell Line, Tumor
- Cell Survival
(drug effects, physiology)
- DNA
(metabolism)
- Dose-Response Relationship, Drug
- G-Quadruplexes
- Guanosine
(metabolism)
- Humans
- Ligands
- Mitochondria
(drug effects, enzymology, physiology)
- Nasopharyngeal Neoplasms
(enzymology, pathology)
- Telomerase
(antagonists & inhibitors, metabolism)
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