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Signal-dependent regulation of gene expression as a target for cancer treatment: inhibiting p38alpha in colorectal tumors.

Abstract：

:In the last year, several evidences indicated that pharmacological manipulation of relevant signaling pathways could selectively affect gene expression to influence cell fate. These findings render of extreme importance the elucidation of how external stimuli are transduced to mediate chromatin modifications, resulting in a permissive or repressive environment for gene expression. These signaling cascades activate or repress the function of chromatin binding proteins that represent attractive pharmacological targets for human diseases. Actually, the closer the target is to chromatin, the more the transcriptional effect will be selective. Recent studies suggest that pharmacological manipulation of signaling pathways to modulate cell fate is indeed possible and that chromatin-associated kinases could represent an optimal target. The p38 MAPK is the prototype of this class of enzymes and its central role in the transcription process is evolutionary conserved. In this review we will focus on the possibility to inhibit p38alpha in colorectal cancer to arrest tumor progression and induce autophagic cell death.

journal_name

Cancer Lett

journal_title

Cancer letters

authors

Chiacchiera F,Simone C

doi

10.1016/j.canlet.2008.02.061

subject

Has Abstract

pub_date

2008-06-28 00:00:00

pages

16-26

issue

1

eissn

0304-3835

issn

1872-7980

pii

S0304-3835(08)00155-9

journal_volume

265

pub_type

杂志文章,评审

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