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Ha-rasVal12 oncogene increases susceptibility of NIH/3T3 cells to lovastatin

Chang, M Y ; Jan, M S ; Won, S J ; Liu, H S

Biochemical and biophysical research communications, 09 July 1998, Vol.248(1), pp.62-8 [Periódico revisado por pares]

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  • Título:
    Ha-rasVal12 oncogene increases susceptibility of NIH/3T3 cells to lovastatin
  • Autor: Chang, M Y ; Jan, M S ; Won, S J ; Liu, H S
  • Assuntos: Apoptosis ; Caspases ; Genes, Ras ; Lovastatin -- Pharmacology
  • É parte de: Biochemical and biophysical research communications, 09 July 1998, Vol.248(1), pp.62-8
  • Descrição: This study demonstrates that Ha-rasVal12 oncogene overexpression sensitizes NIH/3T3 fibroblasts to lovastatin (LOV) cytotoxicity. This sensitization is through apoptosis, which was characterized by increasing CPP32 (caspase-3) activity and DNA fragmentation. Bcl-2 overexpression increased the resistance of the Ha-ras transformants to LOV and rescued the cells from apoptosis, further confirming that the LOV-sensitive cells died of apoptosis. Further analysis showed that Ha-ras activity inversely correlated with WAF1 activity. LOV treatment suppressed Ha-ras activity but induced WAF1 activity and disrupted the cell population in G0/G1 and S phases. The Ha-ras transformants expressing either dominant negative RasAsn17 or Raf-1CB4 showed reverted susceptibility to LOV. These data confirm the involvement of Ras and demonstrate that Raf-1 signalling is required for LOV-induced cell death. Taken together, the possible action of LOV-induced apoptosis is through suppressing Ha-ras activity and increasing...
  • Idioma: Inglês

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