Galangin increases the cytotoxic activity of imatinib mesylate in imatinib-sensitive and imatinib-resistant Bcr-Abl expressing leukemia cells

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Abstract

Resistance to imatinib mesylate is an emergent problem in the treatment of Bcr-Abl expressing myelogenous leukemiasand additional therapeutic strategies are required. We observed that galangin, a non-toxic, naturally occurring flavonoidwas effective as anti-proliferative, and apoptotic agent in Bcr-Abl expressing K562 and KCL22 cells and in imatinib mesylateresistant K562-R and KCL22-R cells. Galangin induced an arrest of cells in G0–G1phase of cell cycle and a decreasein pRb, cdk4, cdk1, cycline B levels; moreover, it was able to induce a monocytic differentiation of leukemic Bcr-Abl+cells. Of note, galangin caused a decrease in Bcl-2 levels and markedly increased the apoptotic activity of imatinib bothin sensitive or imatinib-resistant Bcr-Abl+ cell lines. In contrast, flavonoids unable to modify the Bcl-2 intracellular levels,such as fisetin and chrysin, did not increase the apoptotic effect of imatinib. These data suggest that galangin is an interestingcandidate for a combination therapy in the treatment of imatinib-resistant leukemias.
Original languageEnglish
Pages (from-to)289-297
Number of pages9
JournalCancer Letters
Volume265
Publication statusPublished - 2008

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

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