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Increased resistance to cis-diamminedichloroplatinum(II) in NIH 3T3 cells transformed by ras oncogenes

M D Sklar1

  • 1Department of Radiation Oncology, University of Michigan Medical School, Ann Arbor 48109.

Cancer Research
|February 15, 1988
PubMed

Insights

Activated ras oncogenes significantly increase cellular resistance to the anticancer drug cis-diamminedichloroplatinum(II) (CP). This finding may help predict patient response to CP-based chemotherapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Cellular resistance to cis-diamminedichloroplatinum(II) (CP), a platinum-based anticancer drug, is not well understood.
  • Identifying genes that confer CP resistance is crucial for improving cancer treatment efficacy.

Purpose of the Study:

  • To investigate the role of ras oncogenes in cellular resistance to CP.
  • To determine if activated ras genes can predict clinical response to CP.

Main Methods:

  • Mouse NIH 3T3 fibroblasts were transformed with various ras oncogenes (H, K, N) and other oncogenes (v-mos, v-fms).
  • Clonogenic assays were used to assess cellular survival after CP exposure.
  • The 50% inhibitory concentration (IC50) ratios were calculated to quantify CP resistance.

Main Results:

  • NIH 3T3 fibroblasts transformed with missense mutation-activated ras oncogenes showed substantially increased resistance to CP (IC50 ratios of 4.5-8.5).
  • Cells transformed with v-mos, v-fms, or an overexpressed normal ras protooncogene exhibited intermediate resistance (IC50 ratio approx. 2.0).
  • Control cells (pSV2neo plasmid or non-transforming human DNA) showed no difference in CP resistance compared to NIH 3T3.

Conclusions:

  • Activated ras oncogenes significantly enhance cellular resistance to CP in mouse cells.
  • The findings suggest that activated ras genes in human tumors could potentially predict clinical response to CP-based chemotherapy.

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