Ceacam1L Modulates STAT3 Signaling to Control the Proliferation of Glioblastoma-Initiating Cells

Kaneko, Sadahiro; Nakatani, Yuka; Takezaki, Tatsuya; Hide, Takuichiro; Yamashita, Daisuke; Ohtsu, Naoki; Ohnishi, Takanori; Terasaka, Shunsuke; Houkin, Kiyohiro; Kondo, Toru

Ceacam1L Modulates STAT3 Signaling to Control the Proliferation of Glioblastoma-Initiating Cells

Kaneko, Sadahiro; Nakatani, Yuka; Takezaki, Tatsuya et al.

Cancer research, 2015, 75(19), 4224-4234

Permalink : https://hdl.handle.net/2115/62923

このアイテムのアクセス数:995件（2026-10-15 11:26 集計）

閲覧可能ファイル

ファイル	フォーマット	サイズ	閲覧回数	説明
Manuscript	pdf	3.82 MB	719
SupplementaryData	pdf	2.83 MB	531

論文情報

ファイル出力 EndNote Basic出力 Mendeley出力

アクセス権	open access
URI	https://hdl.handle.net/2115/62923
タイトル	Ceacam1L Modulates STAT3 Signaling to Control the Proliferation of Glioblastoma-Initiating Cells
その他のタイトル	Ceacam1L as a new GIC regulator
著者	Kaneko, Sadahiro ; Nakatani, Yuka ; Takezaki, Tatsuya ; Hide, Takuichiro ; Yamashita, Daisuke ; Ohtsu, Naoki ; Ohnishi, Takanori ; Terasaka, Shunsuke ; Houkin, Kiyohiro ; Kondo, Toru
著者名 Kaneko, Sadahiro
著者名 Nakatani, Yuka
著者名 Takezaki, Tatsuya
e-Rad_Researcher 40421820 著者名 Hide, Takuichiro
著者名 Yamashita, Daisuke
著者名 Ohtsu, Naoki
e-Rad_Researcher 70233210 著者名 Ohnishi, Takanori
e-Rad_Researcher 10447055 著者名 Terasaka, Shunsuke
e-Rad_Researcher 90229146 著者名 Houkin, Kiyohiro
e-Rad_Researcher 30270573 著者名 Kondo, Toru
言語	英語
キーワード	Glioblastoma (GBM)
	GBM-initiating cells (GICs)
	Ceacam1L
	c-Src
	STAT3
発行日	2015-10-01
出版者	American Association for Cancer Research
収録物名	Cancer research
巻(号)	75(19)
ページ	4224-4234
抄録	Glioblastoma-initiating cells (GIC) are a tumorigenic cell subpopulation resistant to radiotherapy and chemotherapy, and are a likely source of recurrence. However, the basis through which GICs are maintained has yet to be elucidated in detail. We herein demonstrated that the carcinoembryonic antigen-related cell adhesion molecule Ceacam1L acts as a crucial factor in GIC maintenance and tumorigenesis by activating c-Src/STAT3 signaling. Furthermore, we showed that monomers of the cytoplasmic domain of Ceacam1L bound to c-Src and STAT3 and induced their phosphorylation, whereas oligomerization of this domain ablated this function. Our results suggest that Ceacam1L-dependent adhesion between GIC and surrounding cells play an essential role in GIC maintenance and proliferation, as mediated by signals transmitted by monomeric forms of the Ceacam1L cytoplasmic domain.
資源タイプ	学術雑誌論文
出版タイプ	Accepted Manuscript
PISSN	0008-5472
NCID	AA00598557
関連情報	PMID 26238781
関連情報 (isVersionOf)	出版社版DOI https://doi.org/10.1158/0008-5472.CAN-15-0412