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MiR‐30a increases MDSC differentiation and immunosuppressive function by targeting SOCS 3 in mice with B‐cell lymphoma
Author(s) -
Xu Zhen,
Ji Jianjian,
Xu Jingjing,
Li Dan,
Shi Guoping,
Liu Fei,
Ding Liang,
Ren Jing,
Dou Huan,
Wang Tingting,
Hou Yayi
Publication year - 2017
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.14133
Subject(s) - stat protein , janus kinase , myeloid derived suppressor cell , chemistry , stat , cancer research , stat3 , signal transduction , t cell , microbiology and biotechnology , immunology , suppressor , biology , immune system , biochemistry , gene
Myeloid‐derived suppressor cells ( MDSC s), including granulocytic (G)‐ MDSC s and monocytic (M)‐ MDSC s, play a critical role in tumor‐induced T cell tolerance. MDSC immunosuppressive function and differentiation are significantly promoted in patients and B‐cell lymphoma model mice. However, the mechanisms regulating these processes remain largely unclear. In the present study, we observed increased micro RNA (miR)‐30a expression both in G‐ MDSC s and in M‐ MDSC s from B cell lymphoma model mice. After transfection with miR‐30a mimics, the differentiation and suppressive capacities of MDSC s were significantly increased via up‐regulation of arginase‐1. Moreover, we showed that the 3′‐ UTR of suppressor of cytokine signaling 3 ( SOCS 3) mRNA is a direct target of miR‐30a. Decreased SOCS 3 expression and activated Janus kinase‐signal transducer and activator of transcription 3 signaling promote MDSC differentiation and suppressive activities. These findings provide new insights into the molecular mechanisms underlying MDSC expansion and function during B cell lymphoma development.