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Zinc-finger transcription factor slug contributes to the survival advantage of chronic myeloid leukemia cells.

Abstract：

:Slug, a Snail-related zinc-finger transcription factor implicated in the increased motility of mesenchymal cells during embryonic development and progression of cancer cells towards an invasive phenotype, plays a specific and critical role in the pathogenesis of Bcr-Abl-associated leukemias. Here we report that Slug over-expression associated with Bcr-Abl is conditional upon the tyrosine kinase (TK) activity of 210 fusion protein. Slug over-expression is driven by transcriptional events eventually integrated by post-transcriptional mechanisms leading to protein stabilization and is at least partly regulated by the ERK1/2 mitogen-activated protein kinase (MAPK). It contributes to apoptosis resistance of leukemic progenitors through the repression of pro-apoptotic Puma. Moreover, Slug is a component of leukemic progenitor resistance to imatinib mesylate (IM) driven by Bcr-Abl point mutations and, in particular, by T315I. Slug over-expression associated with p210 Bcr-Abl TK either in the wild type (wt) or mutated conformation results in a significant reduction of E-cadherin, the substrate of Beta catenin at cell membranes. In conclusion, our results suggest that Slug has a central role in a complex network involved in prolonged survival and IM resistance of CML progenitors.

journal_name

Cell Signal

journal_title

Cellular signalling

authors

Mancini M,Petta S,Iacobucci I,Salvestrini V,Barbieri E,Santucci MA

doi

10.1016/j.cellsig.2010.04.002

subject

Has Abstract

pub_date

2010-08-01 00:00:00

pages

1247-53

issue

8

eissn

0898-6568

issn

1873-3913

pii

S0898-6568(10)00096-3

journal_volume

22

pub_type

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