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Cell Rep. 2012 Feb 23;1(2):141-54. doi: 10.1016/j.celrep.2011.12.005. Epub 2012 Feb 9.

miR-511-3p modulates genetic programs of tumor-associated macrophages.

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  • 1Angiogenesis and Tumor Targeting Unit, and HSR-TIGET, Division of Regenerative Medicine, San Raffaele Institute, 20132-Milan, Italy.

Abstract

Expression of the mannose receptor (MRC1/CD206) identifies macrophage subtypes, such as alternatively activated macrophages (AAMs) and M2-polarized tumor-associated macrophages (TAMs), which are endowed with tissue-remodeling, proangiogenic, and protumoral activity. However, the significance of MRC1 expression for TAM's protumoral activity is unclear. Here, we describe and characterize miR-511-3p, an intronic microRNA (miRNA) encoded by both mouse and human MRC1 genes. By using sensitive miRNA reporter vectors, we demonstrate robust expression and bioactivity of miR-511-3p in MRC1(+) AAMs and TAMs. Unexpectedly, enforced expression of miR-511-3p tuned down the protumoral gene signature of MRC1(+) TAMs and inhibited tumor growth. Our findings suggest that transcriptional activation of Mrc1 in TAMs evokes a genetic program orchestrated by miR-511-3p, which limits rather than enhances their protumoral functions. Besides uncovering a role for MRC1 as gatekeeper of TAM's protumoral genetic programs, these observations suggest that endogenous miRNAs may operate to establish thresholds for inflammatory cell activation in tumors.

Copyright © 2012 The Authors. Published by Elsevier Inc. All rights reserved.

PMID:
22832163
[PubMed - indexed for MEDLINE]
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