Analysis of various mRNA potentially involved in cisplatin resistance of murine leukemia L1210 cells.
Enhanced DNA repair has been identified as a major mechanism of resistance to the anticancer drug cisplatin in murine leukemia L1210 cells. Studies of other cells have implicated the elevation of a variety of RNA transcripts in cisplatin resistance. This study investigated potential changes in transcription of these genes as well as genes involved in DNA repair. No elevation in any of the following transcripts was observed: thymidylate synthase, dihydrofolate reductase, DNA polymerase alpha, DNA polymerase beta, topoisomerase II, Ha-ras, beta-tubulin, metallothionein and the DNA repair genes ERCC1 and ERCC2. Thymidine kinase was increased no more than 2-fold. None of these RNA were induced by incubation with cisplatin. High levels of cisplatin produced selective decreases in certain RNA. These results demonstrate that the previous observations of elevated RNA can not be universally applied to all cisplatin-resistant cells.
Sheibani
N
N
Department of Pharmacology and Toxicology, Dartmouth Medical School, Hanover, NH 03756.
Eastman
A
A
D000818:Animals; D002945:Cisplatin / Q000494:pharmacology*; D004351:Drug Resistance / Q000235:genetics*; D015870:Gene Expression / Q000187:drug effects; D007939:Leukemia L1210 / Q000378:metabolism; D051379:Mice; D011061:Poly A / Q000235:genetics / Q000302:isolation & purification; D012333:RNA, Messenger / Q000187:drug effects / Q000235:genetics* / Q000302:isolation & purification; D014158:Transcription, Genetic / Q000187:drug effects*; D014407:Tumor Cells, Cultured / Q000187:drug effects / Q000378:metabolism*
D012333:RNA, Messenger; D011061:Poly A; D002945:Cisplatin