Telomerase inhibition by non-nucleosidic compound BIBR1532 causes rapid cell death in pre-B acute lymphoblastic leukemia cells.

Abstract:

:Since unlimited proliferative potential has been identified as a major and, to date, therapeutically unexploited phenotypic hallmark of cancer, telomere maintenance mechanisms have been proposed as potential targets for new anticancer interventions. This study was aimed to investigate the effects of BIBR1532, the lead compound of non-nucleosidic inhibition of telomerase, on pre-B acute lymphoblastic leukemia (ALL) cells. BIBR1532 caused rapid cell death in Nalm-6 cells probably through transcriptional suppression of survivin-mediated c-Myc and human telomerase reverse transcriptase (hTERT) expression in a concentration-dependent manner. Moreover, our results also suggest that induced p73, up-regulated Bax/Bcl-2 molecular ratio and subsequent activation of caspase-3 may contribute to a direct short-term cytotoxic effect of high doses of BIBR1532, independent of long-term substantial telomere erosion-mediated cell cycle arrest.

journal_name

Leuk Lymphoma

journal_title

Leukemia & lymphoma

authors

Bashash D,Ghaffari SH,Mirzaee R,Alimoghaddam K,Ghavamzadeh A

doi

10.3109/10428194.2012.704034

subject

Has Abstract

pub_date

2013-03-01 00:00:00

pages

561-8

issue

3

eissn

1042-8194

issn

1029-2403

journal_volume

54

pub_type

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