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Title: MiRNA expression variation in primary NK cells treated with TGF-β1      
ID:
PRJNA386164
description:
Human NK cells activity against cancer cells is deeply suppressed by TGF-β1, an immunomodulatory cytokine that is released and activated in the tumor microenvironment. Moreover, our previous data showed that TGF-β1 modifies the chemokine receptor repertoire of NK cells. In particular, it decreases the expression of CX3CR1 that drives these effectors toward peripheral tissues, including tumor sites. In order to identify possible mechanisms mediating chemokine receptors modulation, we analyzed the miRNA profile of TGF-β1-treated primary NK cells. The analysis pointed out miR-27a-5p as a possible modulator of CX3CR1. We demonstrated the functional interaction of miR-27a-5p with the 3’ untranslated region (3’UTR) of CX3CR1 mRNA by two different experimental approaches: by the use of a luciferase assay based on a reporter construct containing the CX3CR1 3’UTR and by transfection of primary NK cells with a miR-27a-5p inhibitor. We also showed that the TGF-β1-mediated increase of miR-27a-5p expression is a consequence of miR-23a-27a-24-2 cluster induction. Finally, we demonstrated that miR-27a-5p down-regulates the surface expression of CX3CR1. Taken together, our data show that TGF-β1 causes CX3CR1 down-regulation in NK cells by inducing mir-27a-5p, which interacts and degrades the CX3CR1 mRNA. Therefore, the present study highlights miR-27a-5p as a player of TGF-β1-mediated modulatory effects. Overall design: Real-time PCR-based miRNA expression profiling. Primary resting NK cells from three donors were treated for 24h with 5 or 40 ng/ml TGF-β1 or were left untreated.
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landingpage: http://www.ncbi.nlm.nih.gov/bioproject/PRJNA386164
authentication:
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authorization:
none
name:
Homo sapiens
ncbiID:
ncbitax:9606
abbreviation:
NCBI
homePage: http://www.ncbi.nlm.nih.gov
ID:
SCR:006472
name:
National Center for Biotechnology Information
homePage: http://www.ncbi.nlm.nih.gov/bioproject
ID:
SCR:004801
name:
NCBI BioProject