Noncanonical K27-Linked Polyubiquitination of TIEG1 Regulates Foxp3 Expression and Tumor Growth | Zendy

Dong-Jun Peng | Zendy; Minghui Zeng | Zendy; Ryuta Muromoto | Zendy; Tadashi Matsuda | Zendy; Kazuya Shimoda | Zendy; Malayannan Subramaniam | Zendy; Thomas C. Spelsberg | Zendy; WeiZen Wei | Zendy; K. Venuprasad | Zendy

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Noncanonical K27-Linked Polyubiquitination of TIEG1 Regulates Foxp3 Expression and Tumor Growth

Author(s) -

Dong-Jun Peng,

Minghui Zeng,

Ryuta Muromoto,

Tadashi Matsuda,

Kazuya Shimoda,

Malayannan Subramaniam,

Thomas C. Spelsberg,

WeiZen Wei,

K. Venuprasad

Publication year - 2011

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.1003801

Subject(s) - cancer research , ubiquitin , chemistry , biology , biochemistry , gene

Earlier, we demonstrated the essential role of Kruppel-like transcription factor, TIEG1, in TGF-β-induced regulatory T cell (Treg) development. In this article, we demonstrate that IL-6, which promotes Th17 development, abrogated TIEG1 nuclear translocation and inhibited TGF-β-induced Treg development. Tyrosine kinase Tyk2-mediated phosphorylation of TIEG1 at Tyr179 promoted noncanonical K-27-linked polyubiquitination, which inhibited TIEG1 nuclear translocation. To test the role of TIEG1-regulated Treg/Th17 development in antitumor immunity, we analyzed TRAMP-C2 tumor growth in TIEG1(-/-) mice. The defective Treg development and elevated Th17 response resulted in enhanced immune reactivity in the tumor and inhibition of TRAMP-C2 tumor growth in TIEG1(-/-) mice. Thus, our results uncovered a novel regulatory mechanism that modulates Tregs and may regulate tumor progression.

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