Research Article

Cellular and Molecular Life Sciences CMLS

, Volume 61, Issue 17, pp 2253-2263

First online:

Global gene expression of fission yeast in response to cisplatin

  • L. GattiAffiliated withIstituto Nazionale Tumori
  • , D. ChenAffiliated withThe Wellcome Trust Sanger Institute
  • , G. L. BerettaAffiliated withIstituto Nazionale Tumori
  • , G. RusticiAffiliated withThe Wellcome Trust Sanger Institute
  • , N. CareniniAffiliated withIstituto Nazionale Tumori
  • , E. CornaAffiliated withIstituto Nazionale Tumori
  • , D. ColangeloAffiliated withUniversità del Piemonte Orientale
  • , F. ZuninoAffiliated withIstituto Nazionale Tumori
  • , J. BählerAffiliated withThe Wellcome Trust Sanger Institute

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The cellular response to the antitumor drug cisplatin is complex, and resistance is widespread. To gain insights into the global transcriptional response and mechanisms of resistance, we used microarrays to examine the fission yeast cell response to cisplatin. In two isogenic strains with differing drug sensitivity, cisplatin activated a stress response involving glutathione-S-transferase, heat shock, and recombinational repair genes. Genes required for proteasome-mediated protein degradation were up-regulated in the sensitive strain, whereas genes for DNA damage recognition/repair and for mitotic progression were induced in the resistant strain. The response to cisplatin overlaps in part with the responses to cadmium and the DNA-damaging agent methylmethane sulfonate. The different gene groups involved in the cellular response to cisplatin help the cells to tolerate and repair DNA damage and to overcome cell cycle blocks. These findings are discussed with respect to known cisplatin response pathways in human cells.

Cisplatin fission yeast transcriptional profile microarray resistance