Low infiltration of tumor-associated macrophages in high c-Myb-expressing breast tumors

Warning

This publication doesn't include Institute of Computer Science. It includes Faculty of Science. Official publication website can be found on muni.cz.
Authors

VOLODKO Nataliya GUTOR Taras PETRONCHAK Orest HULEY Roman DÚCKA Monika ŠMARDA Jan BORSIG Lubor BENEŠ Petr KNOPFOVÁ Lucia

Year of publication 2019
Type Article in Periodical
Magazine / Source Scientific reports
MU Faculty or unit

Faculty of Science

Citation
Web https://www.nature.com/articles/s41598-019-48051-1
Doi http://dx.doi.org/10.1038/s41598-019-48051-1
Keywords c-Myb; breast cancer; metastasis; survival
Description Tumor-associated macrophages (TAMs) are prominent components of tumor stroma that promotes tumorigenesis. Many soluble factors participate in the deleterious cross-talk between TAMs and transformed cells; however mechanisms how tumors orchestrate their production remain relatively unexplored. c-Myb is a transcription factor recently described as a negative regulator of a specific immune signature involved in breast cancer (BC) metastasis. Here we studied whether c-Myb expression is associated with an increased presence of TAMs in human breast tumors. Tumors with high frequency of c-Myb-positive cells have lower density of CD68-positive macrophages. The negative association is reflected by inverse correlation between MYB and CD68/CD163 markers at the mRNA levels in evaluated cohorts of BC patients from public databases, which was found also within the molecular subtypes. In addition, we identified potential MYB-regulated TAMs recruiting factors that in combination with MYB and CD163 provided a valuable clinical multigene predictor for BC relapse. We propose that identified transcription program running in tumor cells with high MYB expression and preventing macrophage accumulation may open new venues towards TAMs targeting and BC therapy.
Related projects:

You are running an old browser version. We recommend updating your browser to its latest version.

More info