Research Papers:

miR-122-SOCS1-JAK2 axis regulates allergic inflammation and allergic inflammation-promoted cellular interactions

Kyeonga Noh, Misun Kim, Youngmi Kim, Hanearl Kim, Hyuna Kim, Jaehwan Byun, Yeongseo Park, Hansoo Lee, Yun Sil Lee, Jongseon Choe, Young Myeong Kim and Dooil Jeoung _

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Oncotarget. 2017; 8:63155-63176. https://doi.org/10.18632/oncotarget.19149

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Kyeonga Noh1,*, Misun Kim1,*, Youngmi Kim1,*, Hanearl Kim1, Hyuna Kim1, Jaehwan Byun1, Yeongseo Park1, Hansoo Lee2, Yun Sil Lee3, Jongseon Choe4, Young Myeong Kim4 and Dooil Jeoung1

1Department of Biochemistry, Kangwon National University, Chunchon 24341, Korea

2Department of Biological Sciences, Kangwon National University, Chunchon 24341, Korea

3College of Pharmacy, Ewha Womans University, Seoul 03760, Korea

4Graduate School of Medicine, Kangwon National University, Chunchon 24341, Korea

*These authors have contributed equally to this work

Correspondence to:

Dooil Jeoung, email: [email protected]

Keywords: allergic inflammation, cellular interaction, miR-122, SOCS1, tumor microenvironments

Received: December 09, 2016    Accepted: June 19, 2017    Published: July 10, 2017


The regulatory role of suppressor of cytokine signaling 1 (SOCS1) in inflammation has been reported. However, its role in allergic inflammation has not been previously reported. SOCS1 mediated in vitro and in vivo allergic inflammation. Histone deacetylase-3 (HDAC3), a mediator of allergic inflammation, interacted with SOCS1, and miR-384 inhibitor, a positive regulator of HDAC3, induced features of allergic inflammation in an SOCS1-dependent manner. miRNA array analysis showed that the expression of miR-122 was decreased by antigen-stimulation. TargetScan analysis predicted the binding of miR-122 to the 3′-UTR of SOCS1. miR-122 inhibitor induced in vitro and in vivo allergic features in SOCS1-dependent manner. SOCS1 was necessary for allergic inflammation-promoted enhanced tumorigenic and metastatic potential of cancer cells. SOCS1 and miR-122 regulated cellular interactions involving cancer cells, mast cells and macrophages during allergic inflammation. SOCS1 mimetic peptide, D-T-H-F-R-T-F-R-S-H-S-D-Y-R-R-I, inhibited in vitro and in vivo allergic inflammation, allergic inflammation-promoted enhanced tumorigenic and metastatic potential of cancer cells, and cellular interactions during allergic inflammation. Janus kinase 2 (JAK2) exhibited binding to SOCS1 mimetic peptide and mediated allergic inflammation. Transforming growth factor- ß1 (TGF-ß1) was decreased during allergic inflammation and showed an anti-allergic effect. SOCS1 and JAK2 regulated the production of anti-allergic TGF-ß1. Taken together, our results show that miR-122-SOCS1 feedback loop can be employed as a target for the development of anti-allergic and anti-cancer drugs.

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