decitabine and saha-induced apoptosis is accompanied by survivin downregulation and potentiated by atra in p53-deficient cells

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ID: 237487
2014
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Abstract
While p53-dependent apoptosis is triggered by combination of methyltransferase inhibitor decitabine (DAC) and histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) in leukemic cell line CML-T1, reactive oxygen species (ROS) generation as well as survivin and Bcl-2 deregulation participated in DAC + SAHA-induced apoptosis in p53-deficient HL-60 cell line. Moreover, decrease of survivin expression level is accompanied by its delocalization from centromere-related position in mitotic cells suggesting that both antiapoptotic and cell cycle regulation roles of survivin are affected by DAC + SAHA action. Addition of subtoxic concentration of all-trans-retinoic acid (ATRA) increases the efficiency of DAC + SAHA combination on viability, apoptosis induction, and ROS generation in HL-60 cells but has no effect in CML-T1 cell line. Peripheral blood lymphocytes from healthy donors showed no damage induced by DAC + SAHA + ATRA combination. Therefore, combination of ATRA with DAC and SAHA represents promising tool for therapy of leukemic disease with nonfunctional p53 signalization.
Reference Key
brodsk2014oxidativedecitabine Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Barbora Brodská;Petra Otevřelová;Aleš Holoubek
Journal journal of aoac international
Year 2014
DOI
10.1155/2014/165303
URL
http://dx.doi.org/10.1155/2014/165303
Keywords
cytology

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