J 2018

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

KNOPFOVÁ, Lucia, Elisabetta BIGLIERI, Natalya VOLODKO, Michal MASAŘÍK, Markéta HERMANOVÁ et. al.

Basic information

Original name

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

Authors

KNOPFOVÁ, Lucia (203 Czech Republic, guarantor, belonging to the institution), Elisabetta BIGLIERI (380 Italy), Natalya VOLODKO (804 Ukraine), Michal MASAŘÍK (203 Czech Republic, belonging to the institution), Markéta HERMANOVÁ (203 Czech Republic, belonging to the institution), Jesus Francisco GLAUS GARZÓN (756 Switzerland), Monika DÚCKA (703 Slovakia, belonging to the institution), Tereza KUČÍRKOVÁ (203 Czech Republic, belonging to the institution), Karel SOUČEK (203 Czech Republic, belonging to the institution), Jan ŠMARDA (203 Czech Republic, belonging to the institution), Petr BENEŠ (203 Czech Republic, belonging to the institution) and Lubor BORSIG (703 Slovakia)

Edition

Oncogene, London, Nature Publishing Group, 2018, 0950-9232

Other information

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

10601 Cell biology

Country of publisher

United Kingdom of Great Britain and Northern Ireland

Confidentiality degree

není předmětem státního či obchodního tajemství

References:

Impact factor

Impact factor: 6.634

RIV identification code

RIV/00216224:14310/18:00100761

Organization unit

Faculty of Science

UT WoS

000425905700005

Keywords (in Czech)

Myb; endotel; zánět; Ccl2; metastáza; prsní nádory

Keywords in English

Myb; endothelium; inflammation; Ccl2; metastasis; breast cancer

Tags

International impact, Reviewed
Změněno: 23/4/2024 10:49, Mgr. Michal Petr

Abstract

V originále

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.

Links

GJ17-08985Y, research and development project
Name: Prozánětlivá signalizace pod kontrolou proteinu c-Myb v bazálních prsních karcinomech
Investor: Czech Science Foundation
IZ73Z0_152361/1, interní kód MU
Name: c-Myb and Ruk/CIN85 modulate the signaling in breast cancer thereby affecting metastasis (Acronym: c-Myb and Ruk/CIN85 signaling affects metastasis)
Investor: Ostatní - foreign, SCOPES - Scientific Co-operation between Eastern Europe and Switzerland