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Ecrg4 contributes to the anti-glioma immunosurveillance through type-I interferon signaling

OncoImmunology5_e1242547.pdf11.23 MBPDF見る/開く

タイトル: Ecrg4 contributes to the anti-glioma immunosurveillance through type-I interferon signaling
著者: Moriguchi, Tetsuo 著作を一覧する
Kaneumi, Shun 著作を一覧する
Takeda, Shuji 著作を一覧する
Enomoto, Kei 著作を一覧する
Mishra, Shyam Kumar 著作を一覧する
Miki, Tetsuro 著作を一覧する
Koshimizu, Uichi 著作を一覧する
Kitamura, Hidemitsu 著作を一覧する
Kondo, Toru 著作を一覧する
キーワード: Ecrg4
type-I IFN
発行日: 2016年
出版者: Taylor & Francis
誌名: Oncoimmunology
巻: 5
号: 12
開始ページ: e1242547
出版社 DOI: 10.1080/2162402X.2016.1242547
抄録: Esophageal cancer-related gene 4 (Ecrg4), a hormone-like peptide, is thought to be a tumor suppressor, however, little is known about the mechanism of how Ecrg4 suppresses tumorigenesis. Here, we show that the ecrg4 null glioma-initiating cell (GIC) line, which was generated from neural stem cells of ecrg4 knockout (KO) mice, effectively formed tumors in the brains of immunocompetent mice, whereas the transplanted ecrg4 wild type-GIC line GIC(+/+) was frequently eliminated. This was caused by host immune system including adaptive T cell responses, since depletion of CD4+, CD8+, or NK cells by specific antibodies in vivo recovered tumorigenicity of GIC(+/+). We demonstrate that Ecrg4 fragments, amino acid residues 71-132 and 133-148, which are produced by the proteolitic cleavage, induced the expression of pro-inflammatory cytokines in microglia in vitro. Moreover, blockades of type-I interferon (IFN) signaling in vivo, either depleting IFN-α/β receptor 1 or using stat1 KO mice, abrogated the Ecrg4-dependent antitumor activity. Together, our findings indicate a major antitumor function of Ecrg4 in enhancing host immunity via type-I IFN signaling, and suggest its potential as a clinical candidate for cancer immunotherapy.
Rights: This is an Accepted Manuscript of an article published by Taylor & Francis in OncoImmunology in 2016, available online:
資料タイプ: article (author version)
出現コレクション:雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

提供者: 森口 徹生


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