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

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Title: CRKL plays a pivotal role in tumorigenesis of head and neck squamous cell carcinoma through the regulation of cell adhesion
Authors: Yanagi, Hiroko Browse this author
Wang, Lei Browse this author
Nishihara, Hiroshi Browse this author →KAKEN DB
Kimura, Taichi Browse this author →KAKEN DB
Tanino, Mishie Browse this author
Yanagi, Teruki Browse this author
Fukuda, Satoshi Browse this author
Tanaka, Shinya Browse this author →KAKEN DB
Keywords: CRKL
Head and neck squamous cell carcinoma
C3G
Tumorigenesis
CRK
Issue Date: 3-Feb-2012
Publisher: ACADEMIC PRESS INC ELSEVIER SCIENCE
Journal Title: BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume: 418
Issue: 1
Start Page: 104
End Page: 109
Publisher DOI: 10.1016/j.bbrc.2011.12.142
PMID: 22244889
Abstract: 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.
Type: article (author version)
URI: http://hdl.handle.net/2115/51722
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 西原 広史

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