Caracterización del proceso de muerte celular inducido por los derivados bisacilimidoselenocarbamato

• Autores: Iranzu Lamberto Pérez
• Directores de la Tesis: Juan Antonio Palop Cubillo (dir. tes.), Ignacio Encio García (codir. tes.)
• Lectura: En la Universidad de Navarra ( España ) en 2012
• Idioma: español
• Tribunal Calificador de la Tesis: María Luisa Campo Guinea (presid.), Paul Alain Nguewa Tchinda (secret.), Víctor Martínez Merino (voc.), María Jesús López Zabalza (voc.), Almudena Porras Gallo (voc.)
• Materias:
  • Química
    • Bioquímica
    • Química orgánica
  • Ciencias de la vida
    • Biología celular
      • Cultivo celular
    • Biología molecular
• Enlaces
  • Tesis en acceso abierto en: Dadun
• Resumen

  • CHARACTERIZATION OF THE CELL DEATH PROCESS INDUCED BY BISACYLIMIDOSELENOCARBAMATE DERIVATIVES Bisacylimidoselenocarbamate derivatives (BSC) are potent anticancer agents with a strong cytotoxic activity against different types of tumour cells. Based in phosphatidylserine exposure on the cell membranes we show that BSC treatment resulted in enhanced cell death in leukaemia CCRF-CEM cells. DNA fragmentation detection in breast adenocarcinoma MCF-7 cells showed that BSC triggered cell death is concentration and time dependent. We also show that two of these compounds, BSC 3g and 3n, cause cell-cycle arrest in the late G2/M in MCF-7 cells. Consistent with this, a reduction in CDK1 and CDK2 expression with no change in cyclin A and B1 was observed in this cell line. Activation of caspase-2 was also detected. However, the involvement of the caspase-dependent pathway in the process of cell death induced by either BSC 3g or 3n is discarded since cell death could not be prevented by pretreatment with the pancaspase inhibitor z-VAD-fmk. Moreover, since reduced levels of p21CIP and Chk2 proteins but no change in p53 levels could be detected in MCF-7 cells after BSC 3g or 3n treatment our results suggest that BSC treated cells die from lethal mitosis.