Raue, R.R.RaueFrank, A.-C.A.-C.FrankFuhrmann, D.C.D.C.FuhrmannCruz-Ojeda, P. de laP. de laCruz-OjedaRösser, S.S.RösserBauer, R.R.BauerCardamone, G.G.CardamoneWeigert, A.A.WeigertSyed, S.N.S.N.SyedSchmid, T.T.SchmidBrüne, BernhardBernhardBrüne2022-11-292022-11-292022https://publica.fraunhofer.de/handle/publica/42934210.3390/biology110303492-s2.0-85125271681Macrophages constitute a major part of the tumor-infiltrating immune cells. Within the tumor microenvironment, they acquire an alternatively activated, tumor-supporting phenotype. Factors released by tumor cells are crucial for the recruitment of tumor-associated macrophages. In the present project, we aimed to understand the role of hsa-miR-200c-3p (miR-200c) in the interplay between tumor cells and macrophages. To this end, we employed a coculture system of MCF7 breast tumor cells and primary human macrophages and observed the transfer of miR-200c from apoptotic tumor cells to macrophages, which required intact CD36 receptor in macrophages. We further comprehensively determined miR-200c targets in macrophages by mRNA-sequencing and identified numerous migration-associated mRNAs to be downregulated by miR-200c. Consequently, miR-200c attenuated macrophage infiltration into 3-dimensional tumor spheroids. miR-200c-mediated reduction in infiltration further correlated with a miR-200c migration signature comprised of the four miR-200c-repressed, predicted targets PPM1F, RAB11FIB2, RDX, and MSN.enBreast tumorMacrophageMiRTumor microenvironmentjournal article