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Updated: Sep 13, 2026

A Human Glioblastoma Organotypic Slice Culture Model for Study of Tumor Cell Migration and Patient-specific Effects of Anti-Invasive Drugs
Published on: July 20, 2017
CrkI adapter protein modulates cell migration and invasion in glioblastoma
Takahisa Takino1, Mitsutoshi Nakada, Hisashi Miyamori
1Department of Molecular Virology and Oncology, Cancer Research Institute, Graduate School of Medical Science, Kanazawa University, Japan. ttakino@kenroku.kanazawa-u.ac.jp
Abstract:
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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