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Tumor Biology |
Departments of Molecular Virology and Oncology, Cancer Research Institute [T. T., H. M., H. S.], and Neurosurgery, Division of Neuroscience [M. N., J. Y.], Graduate School of Medical Science, Kanazawa University, Kanazawa 920-0934, Japan, and Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental and Craniofacial Research, NIH, Bethesda, Maryland 20892-4370 [K. M. Y.]
The human crk gene is translated into crkI and crkII by alternative splicing. crkII mRNA was detected both in normal brain and glioblastoma tissues, whereas crkI mRNA levels were quite low in normal brain and up-regulated in glioblastoma tissues. Expression of CrkI but not CrkII in glioblastoma U87MG cells induced transformation that stimulated cell migration and invasion concomitant with tyrosine phosphorylation of p130 Crk-associated substrate. N-cadherin-mediated signal transduction, which was essential for invasion by U87MG cells, was no longer required for CrkI-transformed cells. These results suggest that CrkI contributes to malignancy of glioblastoma by inducing phosphorylation of p130 Crk-associated substrate.
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