Detailed Information on Publication Record
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 |
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IZ73Z0_152361/1, interní kód MU |
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