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Rossi, Marco; Altomare, Emanuela; Botta, Cirino; Gallo Cantafio, Maria Eugenia; Sarvide, Sarai; Caracciolo, Daniele; Riillo, Caterina; Gaspari, Marco; Taverna, Domenico; Conforti, Francesco; Critelli, Paola; Bertucci, Bernardo; Iannone, Michelangelo; Polerà, Nicoletta; Scumaci, Domenica; Arbitrio, Mariamena; Amodio, Nicola; Di Martino, Maria Teresa; Paiva, Bruno; Tagliaferri, Pierosandro; Tassone, Pierfrancesco
Leukemia, 03/2021, Volume: 35, Issue: 3Journal Article
Multiple myeloma (MM) is tightly dependent on inflammatory bone marrow microenvironment. IL-17 producing CD4+ T cells (Th17) sustain MM cells growth and osteoclasts-dependent bone damage. In turn, Th17 differentiation relies on inflammatory stimuli. Here, we investigated the role of miR-21 in Th17-mediated MM tumor growth and bone disease. We found that early inhibition of miR-21 in naive T cells (miR-21i-T cells) impaired Th17 differentiation in vitro and abrogated Th17-mediated MM cell proliferation and osteoclasts activity. We validated these findings in NOD/SCID-g-NULL mice, intratibially injected with miR-21i-T cells and MM cells. A Pairwise RNAseq and proteome/phosphoproteome analysis in Th17 cells demonstrated that miR-21 inhibition led to upregulation of STAT-1/-5a-5b, STAT-3 impairment and redirection of Th17 to Th1/Th2 like activated/polarized cells. Our findings disclose the role of miR-21 in pathogenic Th17 activity and open the avenue to the design of miR-21-targeting strategies to counteract microenvironment dependence of MM growth and bone disease.
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