HIC1 Tumor Suppressor Loss Potentiates TLR2/NF-kappa B Signaling and Promotes Tissue Damage-Associated Tumorigenesis

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11310%2F15%3A10321158" target="_blank" >RIV/00216208:11310/15:10321158 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/68378050:_____/15:00455295

Výsledek na webu

<a href="http://dx.doi.org/10.1158/1541-7786.MCR-15-0033" target="_blank" >http://dx.doi.org/10.1158/1541-7786.MCR-15-0033</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1158/1541-7786.MCR-15-0033" target="_blank" >10.1158/1541-7786.MCR-15-0033</a>

Jazyk výsledku

angličtina

Název v původním jazyce

HIC1 Tumor Suppressor Loss Potentiates TLR2/NF-kappa B Signaling and Promotes Tissue Damage-Associated Tumorigenesis

Popis výsledku v původním jazyce

Hypermethylated in cancer 1 (HIC1) represents a prototypic tumor suppressor gene frequently inactivated by DNA methylation in many types of solid tumors. The gene encodes a sequence-specific transcriptional repressor controlling expression of several genes involved in cell cycle or stress control. In this study, a Hic1 allele was conditionally deleted, using a Cre/loxP system, to identify genes influenced by the loss of Hic1. One of the transcripts upregulated upon Hic1 ablation is the toll-like receptor 2 (TLR2). Tlr2 expression levels increased in Hic1-deficient mouse embryonic fibroblasts (MEF) and cultured intestinal organoids or in human cells upon HIC1 knockdown. In addition, HIC1 associated with the TLR2 gene regulatory elements, as detected bychromatin immunoprecipitation, indicating that Tlr2 indeed represents a direct Hic1 target. The Tlr2 receptor senses "danger" signals of microbial or endogenous origin to trigger multiple signaling pathways, including NF-kappa B signaling

Název v anglickém jazyce

HIC1 Tumor Suppressor Loss Potentiates TLR2/NF-kappa B Signaling and Promotes Tissue Damage-Associated Tumorigenesis

Popis výsledku anglicky

Hypermethylated in cancer 1 (HIC1) represents a prototypic tumor suppressor gene frequently inactivated by DNA methylation in many types of solid tumors. The gene encodes a sequence-specific transcriptional repressor controlling expression of several genes involved in cell cycle or stress control. In this study, a Hic1 allele was conditionally deleted, using a Cre/loxP system, to identify genes influenced by the loss of Hic1. One of the transcripts upregulated upon Hic1 ablation is the toll-like receptor 2 (TLR2). Tlr2 expression levels increased in Hic1-deficient mouse embryonic fibroblasts (MEF) and cultured intestinal organoids or in human cells upon HIC1 knockdown. In addition, HIC1 associated with the TLR2 gene regulatory elements, as detected bychromatin immunoprecipitation, indicating that Tlr2 indeed represents a direct Hic1 target. The Tlr2 receptor senses "danger" signals of microbial or endogenous origin to trigger multiple signaling pathways, including NF-kappa B signaling

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

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Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

S - Specificky vyzkum na vysokych skolach

Rok uplatnění

2015

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Molecular Cancer Research

ISSN

1541-7786

e-ISSN

—

Svazek periodika

13

Číslo periodika v rámci svazku

7

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

10

Strana od-do

1139-1148

Kód UT WoS článku

000358059500008

EID výsledku v databázi Scopus

2-s2.0-84942319402