Signaling adaptor protein Crk is indispensable for malignant feature of glioblastoma cell line KMG4

Lei Wang; Kouichi Tabu; Taichi Kimura; Masumi Tsuda; Hua Linghu; Mishie Tanino; Sadao Kaneko; Hiroshi Nishihara; Shinya Tanaka

doi:10.1016/j.bbrc.2007.08.106

Signaling adaptor protein Crk is indispensable for malignant feature of glioblastoma cell line KMG4

Lei Wang, Kouichi Tabu, Taichi Kimura, Masumi Tsuda, Hua Linghu, Mishie Tanino, Sadao Kaneko, Hiroshi Nishihara, Shinya Tanaka

Research output: Contribution to journal › Article › peer-review

37 Citations (Scopus)

Abstract

Signaling adaptor protein Crk has been shown to be involved in pathogenesis of human cancers including brain tumor where Crk was reported to be overexpressed. In this study, we addressed whether Crk is indispensable for malignant phenotype of brain tumor. In 20 surgical specimens of glioma, mRNA of both CrkI and CrkII was found to be elevated in malignant tumor. To define a precise role of Crk, we have established Crk-knockdown cell lines of glioblastoma KMG4 by siRNA, and early phase of cell adhesion to laminin was found to be suppressed. Wound healing assay revealed the decreased cell motility in Crk knockdown cells, and suppression of both anchorage-dependent and -independent growth were demonstrated in these cells. Furthermore, in vivo tumor forming potential was also markedly suppressed. These results suggest that Crk is required for early attachment to laminin, cell motility, and growth of glioblastoma cell line KMG4.

Original language	English
Pages (from-to)	976-981
Number of pages	6
Journal	Biochemical and Biophysical Research Communications
Volume	362
Issue number	4
DOIs	https://doi.org/10.1016/j.bbrc.2007.08.106
Publication status	Published - 2007 Nov 3
Externally published	Yes

Keywords

Adaptor
Adhesion
Brain
Cancer
Crk
Glioblastoma
Invasion
Motility
SH2
Signaling

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.bbrc.2007.08.106

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@article{205685f72c98420f876abe80d796ea69,

title = "Signaling adaptor protein Crk is indispensable for malignant feature of glioblastoma cell line KMG4",

abstract = "Signaling adaptor protein Crk has been shown to be involved in pathogenesis of human cancers including brain tumor where Crk was reported to be overexpressed. In this study, we addressed whether Crk is indispensable for malignant phenotype of brain tumor. In 20 surgical specimens of glioma, mRNA of both CrkI and CrkII was found to be elevated in malignant tumor. To define a precise role of Crk, we have established Crk-knockdown cell lines of glioblastoma KMG4 by siRNA, and early phase of cell adhesion to laminin was found to be suppressed. Wound healing assay revealed the decreased cell motility in Crk knockdown cells, and suppression of both anchorage-dependent and -independent growth were demonstrated in these cells. Furthermore, in vivo tumor forming potential was also markedly suppressed. These results suggest that Crk is required for early attachment to laminin, cell motility, and growth of glioblastoma cell line KMG4.",

keywords = "Adaptor, Adhesion, Brain, Cancer, Crk, Glioblastoma, Invasion, Motility, SH2, Signaling",

author = "Lei Wang and Kouichi Tabu and Taichi Kimura and Masumi Tsuda and Hua Linghu and Mishie Tanino and Sadao Kaneko and Hiroshi Nishihara and Shinya Tanaka",

note = "Funding Information: We thank Miho Nodagashira (Hokkaido University, Japan) for her excellent technical assistances, and Ken Sasai (Hokkaido University, Japan) for critical reading and valuable comments for this manuscript. This study was supported in part by Grants-in-Aid from the Ministry of Education, Science, Culture, and Sports, and from the Ministry of Health, Labor, and Welfare; and also by the YASUDA Medical Research Foundation, by the SUHARA Memorial Foundation, by the Mochida Memorial Foundation for Medical and Pharmaceutical Research, and by the UEHARA Medical Research Foundation. LW was supported by OTOWA Memorial Foundation. ",

year = "2007",

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doi = "10.1016/j.bbrc.2007.08.106",

language = "English",

volume = "362",

pages = "976--981",

journal = "Biochemical and Biophysical Research Communications",

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TY - JOUR

T1 - Signaling adaptor protein Crk is indispensable for malignant feature of glioblastoma cell line KMG4

AU - Wang, Lei

AU - Tabu, Kouichi

AU - Kimura, Taichi

AU - Tsuda, Masumi

AU - Linghu, Hua

AU - Tanino, Mishie

AU - Kaneko, Sadao

AU - Nishihara, Hiroshi

AU - Tanaka, Shinya

N1 - Funding Information: We thank Miho Nodagashira (Hokkaido University, Japan) for her excellent technical assistances, and Ken Sasai (Hokkaido University, Japan) for critical reading and valuable comments for this manuscript. This study was supported in part by Grants-in-Aid from the Ministry of Education, Science, Culture, and Sports, and from the Ministry of Health, Labor, and Welfare; and also by the YASUDA Medical Research Foundation, by the SUHARA Memorial Foundation, by the Mochida Memorial Foundation for Medical and Pharmaceutical Research, and by the UEHARA Medical Research Foundation. LW was supported by OTOWA Memorial Foundation.

PY - 2007/11/3

Y1 - 2007/11/3

N2 - Signaling adaptor protein Crk has been shown to be involved in pathogenesis of human cancers including brain tumor where Crk was reported to be overexpressed. In this study, we addressed whether Crk is indispensable for malignant phenotype of brain tumor. In 20 surgical specimens of glioma, mRNA of both CrkI and CrkII was found to be elevated in malignant tumor. To define a precise role of Crk, we have established Crk-knockdown cell lines of glioblastoma KMG4 by siRNA, and early phase of cell adhesion to laminin was found to be suppressed. Wound healing assay revealed the decreased cell motility in Crk knockdown cells, and suppression of both anchorage-dependent and -independent growth were demonstrated in these cells. Furthermore, in vivo tumor forming potential was also markedly suppressed. These results suggest that Crk is required for early attachment to laminin, cell motility, and growth of glioblastoma cell line KMG4.

AB - Signaling adaptor protein Crk has been shown to be involved in pathogenesis of human cancers including brain tumor where Crk was reported to be overexpressed. In this study, we addressed whether Crk is indispensable for malignant phenotype of brain tumor. In 20 surgical specimens of glioma, mRNA of both CrkI and CrkII was found to be elevated in malignant tumor. To define a precise role of Crk, we have established Crk-knockdown cell lines of glioblastoma KMG4 by siRNA, and early phase of cell adhesion to laminin was found to be suppressed. Wound healing assay revealed the decreased cell motility in Crk knockdown cells, and suppression of both anchorage-dependent and -independent growth were demonstrated in these cells. Furthermore, in vivo tumor forming potential was also markedly suppressed. These results suggest that Crk is required for early attachment to laminin, cell motility, and growth of glioblastoma cell line KMG4.

KW - Adaptor

KW - Adhesion

KW - Brain

KW - Cancer

KW - Crk

KW - Glioblastoma

KW - Invasion

KW - Motility

KW - SH2

KW - Signaling

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SN - 0006-291X

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JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

IS - 4

ER -

Signaling adaptor protein Crk is indispensable for malignant feature of glioblastoma cell line KMG4

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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