CrkI adapter protein modulates cell migration and invasion in glioblastoma.
CrkI adapter protein modulates cell migration and invasion in glioblastoma.
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DOI：
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发表时间：
2003-03
期刊：
影响因子：
11.2
通讯作者：
T. Takino;M. Nakada;H. Miyamori;J. Yamashita;Kenneth M. Yamada;Hiroshi Sato
中科院分区：
文献类型：
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作者：
T. Takino;M. Nakada;H. Miyamori;J. Yamashita;Kenneth M. Yamada;Hiroshi Sato
人的crk基因通过选择性剪接被翻译成crkI和crkII。CrkII在正常脑组织和胶质母细胞瘤组织中均有表达，而在正常脑组织中表达很低，在胶质母细胞瘤组织中表达上调。在胶质母细胞瘤U87 MG细胞中表达CrkI，但不表达CrkII，诱导的转化刺激了细胞的迁移和侵袭，伴随着p130 Crk相关底物的酪氨酸磷酸化。转导CrkI的U87 MG细胞不再需要N-钙粘素介导的侵袭信号转导。这些结果表明，CrkI通过诱导p130Crk相关底物的磷酸化参与了胶质母细胞瘤的恶性转化。
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.