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LBH-589 (panobinostat) potentiates fludarabine anti-leukemic activity through a JNK- and XIAP-dependent mechanism.

Abstract：

:Effects of the HDAC inhibitor LBH-589 (panobinostat) on fludarabine lethality toward acute myeloid leukemia (AML) cells were examined in vitro and in vivo. LBH-589 pretreatment sensitized U937, HL-60, and primary leukemia cells to fludarabine while blocking NF-κB activation accompanied by XIAP down-regulation and JNK activation. Pharmacologic or genetic JNK inhibition significantly attenuated LBH-589/fludarabine lethality, whereas XIAP over-expression diminished JNK activation and apoptosis. Combined in vivo treatment abrogated leukemia growth in a U937 xenograft murine model and substantially increased animal survival. These studies highlight the interplay between NF-κB activation, XIAP down-regulation, and JNK activation in anti-leukemic synergism between fludarabine and LBH-589.

journal_name

Leuk Res

journal_title

Leukemia research

authors

Rosato R,Hock S,Dent P,Dai Y,Grant S

doi

10.1016/j.leukres.2011.10.020

subject

Has Abstract

pub_date

2012-04-01 00:00:00

pages

491-8

issue

4

eissn

0145-2126

issn

1873-5835

pii

S0145-2126(11)00517-0

journal_volume

36

pub_type

杂志文章

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