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

Result code in 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>

Alternative codes found

RIV/68378050:_____/15:00455295

Result on the web

<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>

Result language

angličtina

Original language name

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

Original language description

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

Czech name

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Czech description

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Type

J_x - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

CEP classification

EB - Genetics and molecular biology

OECD FORD branch

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Project

Result was created during the realization of more than one project. More information in the Projects tab.

Continuities

S - Specificky vyzkum na vysokych skolach

Publication year

2015

Confidentiality

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

Name of the periodical

Molecular Cancer Research

ISSN

1541-7786

e-ISSN

—

Volume of the periodical

13

Issue of the periodical within the volume

7

Country of publishing house

US - UNITED STATES

Number of pages

10

Pages from-to

1139-1148

UT code for WoS article

000358059500008

EID of the result in the Scopus database

2-s2.0-84942319402