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Endoplasmic reticulum stress contributes to arsenic trioxide-induced apoptosis in drug-sensitive and -resistant leukemia cells

Chen, Jing ; Wei, Hulai ; Xie, Bei ; Wang, Bei ; Cheng, Juan ; Cheng, Jie

Leukemia Research, December 2012, Vol.36(12), pp.1526-1535 [Periódico revisado por pares]

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  • Título:
    Endoplasmic reticulum stress contributes to arsenic trioxide-induced apoptosis in drug-sensitive and -resistant leukemia cells
  • Autor: Chen, Jing ; Wei, Hulai ; Xie, Bei ; Wang, Bei ; Cheng, Juan ; Cheng, Jie
  • Assuntos: Arsenic Trioxide ; Drug Resistance ; Endoplasmic Reticulum Stress ; Apoptosis ; Arsenic Trioxide ; Drug Resistance ; Endoplasmic Reticulum Stress ; Apoptosis ; Medicine
  • É parte de: Leukemia Research, December 2012, Vol.36(12), pp.1526-1535
  • Descrição: This study characterized the role of endoplasmic reticulum stress (ERS)-related pathways in arsenic trioxide-induced apoptosis in multidrug-resistant leukemia K562/ADM cells. Arsenic trioxide exposure led to much significant induction of apoptosis in K562/ADM cells than the parental K562 cells, and the chaperone proteins glucose-regulated protein 78, CHOP/GADD153, X-box binding protein-1 and caspase-12 were activated to varying degrees. Furthermore, arsenic trioxide stimulation led to inhibition of P-glycoprotein and Bcl-2 expression. This study demonstrates a missing link between arsenic trioxide and ERS-induced apoptosis, and suggests that the greater effects obtained in drug-resistant K562/ADM cells may be mediated by downregulation of P-glycoprotein and Bcl-2 expression.
  • Idioma: Inglês

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