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

Oncogene
L KnopfováLubor Borsig

Abstract

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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Citations

Sep 19, 2019·Marine Drugs·Jortan O TunGisela P Concepcion
Aug 14, 2019·Scientific Reports·Nataliya VolodkoLucia Knopfová
Feb 24, 2021·Neoplasia : an International Journal for Oncology Research·Monika DúckaLucia Knopfová
Jan 8, 2022·Clinical & Experimental Metastasis·Kamila ŘíhováPetr Beneš

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