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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
1994-10-6
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pubmed:abstractText |
We examined the differential effects of the H-ras oncogene and the K-ras oncogene on cisplatin sensitivity in murine NIH/3T3 cells transfected with these oncogenes. Although the NIH/3T3 cells transformed with H-ras oncogenes (EJ-NIH/3T3 and Ha8-21) showed an increased resistance to cisplatin compared to the parental NIH/3T3, the cell lines transformed with K-ras oncogenes (DT and 1,8DNP2-2-5) did not. Compared with NIH/3T3, the 2 H-ras transformants reduced both the accumulation of cisplatin and the Na+,K(+)-ATPase activity in the membrane fraction. On the other hand, we observed no significant difference in cellular accumulation of cisplatin or in Na+,K(+)-ATPase activity between parental NIH/3T3 and the K-ras transformants. Since these ras transformants did not affect the cellular metallothionein content, transcriptional level of DNA polymerase beta or activity of glutathione-S-transferase which is not associated with cisplatin sensitivity, these results suggest that cisplatin resistance is brought about by the H-ras oncogene, but not by K-ras, and that induction of cisplatin resistance by H-ras is mainly due to a reduction of cisplatin accumulation and an impairment of Na+,K(+)-ATPase activity in the membrane fraction.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cisplatin,
http://linkedlifedata.com/resource/pubmed/chemical/DNA Polymerase I,
http://linkedlifedata.com/resource/pubmed/chemical/Glutathione Transferase,
http://linkedlifedata.com/resource/pubmed/chemical/Metallothionein,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins p21(ras),
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Neoplasm,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Potassium-Exchanging ATPase
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0020-7136
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
58
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pubmed:geneSymbol |
H-ras,
K-ras
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
672-7
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:8077052-3T3 Cells,
pubmed-meshheading:8077052-Animals,
pubmed-meshheading:8077052-Cell Survival,
pubmed-meshheading:8077052-Cell Transformation, Neoplastic,
pubmed-meshheading:8077052-Cisplatin,
pubmed-meshheading:8077052-DNA Polymerase I,
pubmed-meshheading:8077052-Genes, ras,
pubmed-meshheading:8077052-Glutathione Transferase,
pubmed-meshheading:8077052-Metallothionein,
pubmed-meshheading:8077052-Mice,
pubmed-meshheading:8077052-Proto-Oncogene Proteins p21(ras),
pubmed-meshheading:8077052-RNA, Messenger,
pubmed-meshheading:8077052-RNA, Neoplasm,
pubmed-meshheading:8077052-Sodium-Potassium-Exchanging ATPase
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pubmed:year |
1994
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pubmed:articleTitle |
Differential Na+,K(+)-ATPase activity and cisplatin sensitivity between transformants induced by H-ras and those induced by K-ras.
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pubmed:affiliation |
Department of Urology, Hokkaido University School of Medicine, Sapporo, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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