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

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Publikace nespadá pod Fakultu sportovních studií, ale pod Přírodovědeckou fakultu. Oficiální stránka publikace je na webu muni.cz.
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KNOPFOVÁ Lucia BIGLIERI Elisabetta VOLODKO Natalya MASAŘÍK Michal HERMANOVÁ Markéta GLAUS GARZÓN Jesus Francisco DÚCKA Monika KUČÍRKOVÁ Tereza SOUČEK Karel ŠMARDA Jan BENEŠ Petr BORSIG Lubor

Rok publikování 2018
Druh Článek v odborném periodiku
Časopis / Zdroj Oncogene
Fakulta / Pracoviště MU

Přírodovědecká fakulta

Citace
www http://dx.doi.org/10.1038/onc.2017.392
Doi http://dx.doi.org/10.1038/onc.2017.392
Obor Genetika a molekulární biologie
Klíčová slova Myb; endothelium; inflammation; Ccl2; metastasis; breast cancer
Popis 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.
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