• Abrogation of histone deacetylases (HDACs) decreases survival of chronic myeloid leukemia cells
  • sara zehtabche,1,*
    1. Shahid Beheshti University of Medical Sciences


  • Introduction: Although the identification of tyrosine kinase inhibitors has changed the treatment paradigm of many cancer types including chronic myeloid leukemia (CML), still adjustment of neoplastic cells to cytotoxic effects of anti-cancer drugs is a serious challenge. In the area of drug resistance, epigenetic alterations are at the center of attention and the present study aimed to evaluate whether blockage of epigenetic mechanisms using a pan-histone deacetylase (HDAC) inhibitor induces cell death in CML-derived K562 cells.
  • Methods: in order to evaluate the effect of Panobinostat on CML cells, K562 cells treated with Panobinostat. then cell survival was evaluated using Trypan blue exclusion assay and MTT assay. The distribution of treated cells in different-phase of cell cycle was evaluated using PI standing.
  • Results: We found that the abrogation of HDACs using panobinostat resulted in a reduction in survival of the K562 cell line through p21-mediated G1 cell cycle arrest.
  • Conclusion: The results of the present study shed new light on the role of HDACs activity on the chemosensitivity of CML cells and suggested panobinostat as an appealing agent in CML treatment strategies.
  • Keywords: CML; Histone deacetylase (HDAC); HDAC inhibition; Panobinostat