Regulation of NFKBIZ gene promoter activity by STAT3, C/EBPβ, and STAT1.

Muromoto, Ryuta; Sato, Ami; Komori, Yuki; Nariya, Kota; Kitai, Yuichi; Kashiwakura, Jun-Ichi; Matsuda, Tadashi

Regulation of NFKBIZ gene promoter activity by STAT3, C/EBPβ, and STAT1.

Muromoto, Ryuta; Sato, Ami; Komori, Yuki et al.

Biochemical and biophysical research communications, 2022, 613, 61-66

Permalink : https://hdl.handle.net/2115/90199

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論文情報

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アクセス権	open access
URI	https://hdl.handle.net/2115/90199
タイトル	Regulation of NFKBIZ gene promoter activity by STAT3, C/EBPβ, and STAT1.
著者	Muromoto, Ryuta ; Sato, Ami ; Komori, Yuki ; Nariya, Kota ; Kitai, Yuichi ; Kashiwakura, Jun-Ichi ; Matsuda, Tadashi
e-Rad_Researcher 30455597 著者名 Muromoto, Ryuta
著者名 Sato, Ami
著者名 Komori, Yuki
著者名 Nariya, Kota
e-Rad_Researcher 90756165 著者名 Kitai, Yuichi
e-Rad_Researcher 90373290 著者名 Kashiwakura, Jun-Ichi
e-Rad_Researcher 20212219 著者名 Matsuda, Tadashi
言語	英語
キーワード	Inflammation
	Cytokine
	STAT
	C/EBPβ
	IκB-ζ
	Transcriptional regulation
発行日	2022-07-12
出版者	Academic Press
出版者	Elsevier
収録物名	Biochemical and biophysical research communications
巻(号)	613
ページ	61-66
抄録	Interleukin-17A (IL-17A) is a cytokine that affects the functions of non-immune cells, including keratinocytes, and thereby amplifies immune responses. An IκB family protein IκB-ζ, encoded by the NFKBIZ gene, mediates IL-17A-induced inflammatory cellular responses. Previously we reported that a transcription factor STAT3 mediates the transcriptional induction of NFKBIZ through its binding to the specific binding site existing in the NFKBIZ promoter. However, it remains unclear how other transcription factors regulate NFKBIZ transcription. Here, we investigated the NFKBIZ promoter regulation by transcription factors C/EBPβ and STAT1 and revealed opposing roles of C/EBPβ and STAT1 in NFKBIZ transcription. We found that siRNA-mediated knockdown of C/EBPβ attenuates IL-17A-induced upregulation of NFKBIZ in the HaCaT cell line. A putative C/EBP-binding site is located adjacent to the STAT-binding site in the NFKBIZ promoter, the deletion of which abolished C/EBPβ-driven promoter activation in transient NFKBIZ promoter-luciferase assay. Deleting the STAT-binding site also led to a reduction in C/EBPβ-driven promoter activation, suggesting a cooperative action between C/EBP- and STAT-binding sites. Furthermore, Co-overexpression of STAT1 suppressed both C/EBPβ- and STAT3-driven NFKBIZ promoter activation independently of its tyrosine 701 phosphorylation. siRNA-mediated STAT1 knockdown augmented IκB-ζ induction in IL-17A-treated HaCaT cells, with enhanced expression of an IκB-ζ target gene DEFB4A. Together, these results indicate that both C/EBPβ and STAT3 are transcription factors that coordinately induce NFKBIZ promoter activation, indicating that STAT1 has an inhibitory role. Thus, these could be a fine-tuning mechanism of IL-17A-IκB-ζ-mediated cellular responses.
資源タイプ	学術雑誌論文
出版タイプ	Accepted Manuscript
権利情報	Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
権利情報	© 2022. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/
PISSN	1090-2104
関連情報	PMID 35537286
関連情報 (isVersionOf)	出版社版DOI https://doi.org/10.1016/j.bbrc.2022.04.140