| pubmed-article:9687575 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9687575 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:9687575 | lifeskim:mentions | umls-concept:C1155661 | lld:lifeskim |
| pubmed-article:9687575 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:9687575 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:9687575 | pubmed:dateCreated | 1998-8-31 | lld:pubmed |
| pubmed-article:9687575 | pubmed:abstractText | Postreplicative mismatch repair plays a major role in mediating the cytotoxicity of agents generating O6-methylguanine in DNA. We previously showed that a methylating antitumor triazene compound, temozolomide, induces apoptosis and that the persistence of O6-methylguanine in DNA is required to trigger the process. We wanted to test whether the latter apoptotic signal is dependent on a functional mismatch repair system. To this end, we used two human lymphoblastoid cell lines (i.e., the mismatch repair-proficient TK6 line and its mismatch repair-deficient subline MT1) that are both deficient in O6-methylguanine repair. Temozolomide treatment of TK6 cells brought about efficient cell growth inhibition, G2/M arrest, and apoptosis, as indicated by the results of cytofluorimetric analysis of 5-bromo-2'-deoxyuridine incorporation and DNA content and evaluation of DNA fragmentation. The drug treatment resulted also in the induction of p53 and p21/waf-1 protein expression. In contrast, MT1 cells were highly resistant to the drug and no p53 and p21/waf-1 induction was observed. Importantly, we could show that MT1 cells are not deficient in the p53-dependent apoptosis pathway; treatment with etoposide, a topoisomerase II inhibitor, resulted in p53 and p21/waf-1 protein expression and apoptosis in both cell lines. In conclusion, we demonstrate the existence of a link between a functional mismatch repair system and the trigger of apoptosis in cells exposed to clinically relevant concentrations of temozolomide. The results also suggest that p53 induction in response to O6-guanine methylation involves the mismatch repair system. | lld:pubmed |
| pubmed-article:9687575 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:9687575 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9687575 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9687575 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:9687575 | pubmed:issn | 0026-895X | lld:pubmed |
| pubmed-article:9687575 | pubmed:author | pubmed-author:GrazianiGG | lld:pubmed |
| pubmed-article:9687575 | pubmed:author | pubmed-author:TentoriLL | lld:pubmed |
| pubmed-article:9687575 | pubmed:author | pubmed-author:BonmassarEE | lld:pubmed |
| pubmed-article:9687575 | pubmed:author | pubmed-author:BenincasaEE | lld:pubmed |
| pubmed-article:9687575 | pubmed:author | pubmed-author:PaganiEE | lld:pubmed |
| pubmed-article:9687575 | pubmed:author | pubmed-author:ZambrunoGG | lld:pubmed |
| pubmed-article:9687575 | pubmed:author | pubmed-author:LacalP MPM | lld:pubmed |
| pubmed-article:9687575 | pubmed:author | pubmed-author:D'AtriSS | lld:pubmed |
| pubmed-article:9687575 | pubmed:author | pubmed-author:JiricnyJJ | lld:pubmed |
| pubmed-article:9687575 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9687575 | pubmed:volume | 54 | lld:pubmed |
| pubmed-article:9687575 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9687575 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9687575 | pubmed:pagination | 334-41 | lld:pubmed |
| pubmed-article:9687575 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:9687575 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9687575 | pubmed:articleTitle | Involvement of the mismatch repair system in temozolomide-induced apoptosis. | lld:pubmed |
| pubmed-article:9687575 | pubmed:affiliation | Istituto Dermopatico Dell'Immacolata, Rome, Italy. s.datri@idi.it | lld:pubmed |
| pubmed-article:9687575 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9687575 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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