CRKL plays a pivotal role in tumorigenesis of head and neck squamous cell carcinoma through the regulation of cell adhesion

Yanagi, Hiroko; Wang, Lei; Nishihara, Hiroshi; Kimura, Taichi; Tanino, Mishie; Yanagi, Teruki; Fukuda, Satoshi; Tanaka, Shinya

CRKL plays a pivotal role in tumorigenesis of head and neck squamous cell carcinoma through the regulation of cell adhesion

Yanagi, Hiroko; Wang, Lei; Nishihara, Hiroshi et al.

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2012, 418(1), 104-109

Permalink : https://hdl.handle.net/2115/51722

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アクセス権	open access
URI	https://hdl.handle.net/2115/51722
タイトル	CRKL plays a pivotal role in tumorigenesis of head and neck squamous cell carcinoma through the regulation of cell adhesion
著者	Yanagi, Hiroko ; Wang, Lei ; Nishihara, Hiroshi ; Kimura, Taichi ; Tanino, Mishie ; Yanagi, Teruki ; Fukuda, Satoshi ; Tanaka, Shinya
著者名 Yanagi, Hiroko
著者名 Wang, Lei
e-Rad_Researcher 50322805 著者名 Nishihara, Hiroshi
e-Rad_Researcher 90435959 著者名 Kimura, Taichi
著者名 Tanino, Mishie
著者名 Yanagi, Teruki
著者名 Fukuda, Satoshi
e-Rad_Researcher 70261287 著者名 Tanaka, Shinya
言語	英語
キーワード	CRKL
	Head and neck squamous cell carcinoma
	C3G
	Tumorigenesis
	CRK
発行日	2012-02-03
出版者	ACADEMIC PRESS INC ELSEVIER SCIENCE
収録物名	BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
巻(号)	418(1)
ページ	104-109
抄録	The signaling adapter protein CRK is an indispensable molecule involved in regulating the malignant potential of human cancers. CRK-like (CRKL) is a hematopoietic cell-dominant homologue of CRK that is reported to be phosphorylated by BCR-ABL tyrosine kinase in chronic myelogenous leukemia patients, but its biological function in non-hematopoietic tumors remains unclear. In this study, we explored the tumorigenic role of CRKL in head and neck squamous cell carcinoma (HNSCC) in vitro and in vivo. Immunoprecipitation analysis of HNSCC cell line, HSC-3 cells, showed that the dominant binding partner for C3G was CRKL, not CRK. To clarify the molecular function of CRKL, we established lentiviral shRNA-mediated CRKL-knockdown HNSCC cell lines. In CRKL-knockdown HSC-3 and HSC-4 cells, cell growth and motility were diminished compared to control cells. Cell adhesion assays showed that cell attachment onto both fibronectin- and collagen-coated dishes was significantly suppressed in CRKL-knockdown HSC-3 cells, while no significant change was observed for poly-L-lysine-coated dishes. Immunofluorescence staining revealed that focal adhesion was reduced in CRKL-knockdown HSC-3 cells. With a pull-down assay, CRKL-knockdown HSC-3 cells showed decreased amounts of active Rap1 compared to control cells. Moreover, in an in vivo assay, tumor formation of CRKL-knockdown HSC-3 cells in nude mice was significantly abrogated. Our results indicate that CRKL regulates HNSCC-cell growth, motility, and integrin-dependent cell adhesion, suggesting that CRKL plays a principal role in HNSCC tumorigenicity. (C) 2012 Elsevier Inc. All rights reserved.
資源タイプ	学術雑誌論文
出版タイプ	Accepted Manuscript
PISSN	0006-291X
関連情報	PMID 22244889
関連情報 (isVersionOf)	出版社版DOI https://doi.org/10.1016/j.bbrc.2011.12.142