Transcription factor c-Myb inhibits breast cancer lung metastasis by suppression of tumor cell seeding

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14310%2F18%3A00100761" target="_blank" >RIV/00216224:14310/18:00100761 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/68081707:_____/18:00488378 RIV/00159816:_____/18:00067441

Výsledek na webu

<a href="http://dx.doi.org/10.1038/onc.2017.392" target="_blank" >http://dx.doi.org/10.1038/onc.2017.392</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1038/onc.2017.392" target="_blank" >10.1038/onc.2017.392</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Transcription factor c-Myb inhibits breast cancer lung metastasis by suppression of tumor cell seeding

Popis výsledku v původním jazyce

Metastasis accounts for most of cancer-related deaths. Paracrine signaling between tumor cells and the stroma induces changes in the tumor microenvironment required for metastasis. Transcription factor c-Myb was associated with breast cancer (BC) progression but its role in metastasis remains unclear. Here we show that increased c-Myb expression in BC cells inhibits spontaneous lung metastasis through impaired tumor cell extravasation. On contrary, BC cells with increased lung metastatic capacity exhibited low c-Myb levels. We identified a specific inflammatory signature, including Ccl2 chemokine; that was expressed in lung metastatic cells but was suppressed in tumor cells with higher c-Myb levels. Tumor cell-derived Ccl2 expression facilitated lung metastasis and rescued trans-endothelial migration of c-Myb overexpressing cells. Clinical data show that the identified inflammatory signature, together with a MYB expression, predicts lung metastasis relapse in BC patients. These results demonstrate that the c-Myb-regulated transcriptional program in BCs results in a blunted inflammatory response and consequently suppresses lung metastasis.

Název v anglickém jazyce

Transcription factor c-Myb inhibits breast cancer lung metastasis by suppression of tumor cell seeding

Popis výsledku anglicky

Metastasis accounts for most of cancer-related deaths. Paracrine signaling between tumor cells and the stroma induces changes in the tumor microenvironment required for metastasis. Transcription factor c-Myb was associated with breast cancer (BC) progression but its role in metastasis remains unclear. Here we show that increased c-Myb expression in BC cells inhibits spontaneous lung metastasis through impaired tumor cell extravasation. On contrary, BC cells with increased lung metastatic capacity exhibited low c-Myb levels. We identified a specific inflammatory signature, including Ccl2 chemokine; that was expressed in lung metastatic cells but was suppressed in tumor cells with higher c-Myb levels. Tumor cell-derived Ccl2 expression facilitated lung metastasis and rescued trans-endothelial migration of c-Myb overexpressing cells. Clinical data show that the identified inflammatory signature, together with a MYB expression, predicts lung metastasis relapse in BC patients. These results demonstrate that the c-Myb-regulated transcriptional program in BCs results in a blunted inflammatory response and consequently suppresses lung metastasis.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10601 - Cell biology

Projekt

<a href="/cs/project/GJ17-08985Y" target="_blank" >GJ17-08985Y: Prozánětlivá signalizace pod kontrolou proteinu c-Myb v bazálních prsních karcinomech</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2018

Kód důvěrnosti údajů

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

Název periodika

Oncogene

ISSN

0950-9232

e-ISSN

—

Svazek periodika

37

Číslo periodika v rámci svazku

8

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

11

Strana od-do

1020-1030

Kód UT WoS článku

000425905700005

EID výsledku v databázi Scopus

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