CrkI衔接蛋白调节胶质母细胞瘤中的细胞迁移和侵袭。
CrkI adapter protein modulates cell migration and invasion in glioblastoma.
作者信息
Takino Takahisa, Nakada Mitsutoshi, Miyamori Hisashi, Yamashita Junkoh, Yamada Kenneth M, Sato Hiroshi
机构信息
Department of Molecular Virology and Oncology, Cancer Research Institute, Graduate School of Medical Science, Kanazawa University, Japan.
出版信息
Cancer Res. 2003 May 1;63(9):2335-7.
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.
人类crk基因通过可变剪接被翻译成crkI和crkII。在正常脑和胶质母细胞瘤组织中均检测到crkII mRNA，而crkI mRNA水平在正常脑中相当低，在胶质母细胞瘤组织中上调。在胶质母细胞瘤U87MG细胞中表达CrkI而非CrkII可诱导细胞转化，刺激细胞迁移和侵袭，并伴随p130 Crk相关底物的酪氨酸磷酸化。U87MG细胞侵袭所必需的N-钙黏蛋白介导的信号转导对于CrkI转化的细胞不再是必需的。这些结果表明，CrkI通过诱导p130 Crk相关底物的磷酸化促进胶质母细胞瘤的恶性发展。
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