| Autor: |
Zhao R; Department of Oncology, Radiumhemmet, Karolinska Hospital, Stockholm, Sweden., Rabo YB, Egyházi S, Andersson A, Edgren MR, Linder S, Hansson J |
| Jazyk: |
angličtina |
| Zdroj: |
Anti-cancer drugs [Anticancer Drugs] 1995 Oct; Vol. 6 (5), pp. 657-68. |
| DOI: |
10.1097/00001813-199510000-00005 |
| Abstrakt: |
Cisplatin resistance was developed in the human melanoma cell line RPMI8322 by repeated short-term exposures to cisplatin. The most resistant daughter cell line, RPMI8322/CDDP-300, was 4-fold resistant to cisplatin, and partially cross-resistant to carboplatin, melphalan and UV, but not to BCNU. RPMI8322/CDDP-300 cells showed less apoptosis after cisplatin than the parental cells. The cisplatin resistance was not paralleled by a similar reduction in cellular cisplatin accumulation or DNA cross-links in RPMI8322/CDDP-300 cells, and these cells exhibited no increase in cellular glutathione or in mRNA encoding the DNA excision repair protein ERCC1 and XPB. Induction of c-jun mRNA by cisplatin was considerably lower in RPMI8322/CDDP-300 cells than in RPMI8322 cells, consistent with the possibility that c-jun induction may be involved in a pathway that triggers apoptosis after exposure to DNA damaging agents. However, c-jun induction is not necessary for apoptosis, since cisplatin also induced apoptosis in A14 rat embryo fibroblasts, cells in which the c-jun gene is deleted. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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