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miR-122-SOCS1-JAK2 axis regulates allergic inflammation and allergic inflammation-promoted cellular interactions
- Title
- miR-122-SOCS1-JAK2 axis regulates allergic inflammation and allergic inflammation-promoted cellular interactions
- Authors
- Noh K.; Kim M.; Kim Y.; Kim H.; Byun J.; Park Y.; Lee H.; Lee Y.S.; Choe J.; Kim Y.M.; Jeoung D.
- Ewha Authors
- 이윤실
- SCOPUS Author ID
- 이윤실
- Issue Date
- 2017
- Journal Title
- Oncotarget
- ISSN
- 1949-2553
- Citation
- Oncotarget vol. 8, no. 38, pp. 63155 - 63176
- Keywords
- Allergic inflammation; Cellular interaction; MiR-122; SOCS1; Tumor microenvironments
- Publisher
- Impact Journals LLC
- Indexed
- SCIE; SCOPUS
- Document Type
- Article
- Abstract
- 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- β1 (TGF-β1) was decreased during allergic inflammation and showed an anti-allergic effect. SOCS1 and JAK2 regulated the production of anti-allergic TGF-β1. 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. © Noh et al.
- DOI
- 10.18632/oncotarget.19149
- Appears in Collections:
- 약학대학 > 약학과 > Journal papers
- Files in This Item:
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