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標題: Focal Adhesion Kinase在致癌基因v-src 所引起的細胞癌化中所扮演的角色
The role of focal adhesion kinase in v-src-induced tumor formation
作者: 謝金玲
Hsieh, Chin-Ling
關鍵字: 細胞轉形;腫瘤生成
出版社: 生物化學研究所
Focal adhesion kinase (FAK) 是一種非受器的酪氨酸磷酸化脢,隨著integrin 調控細胞附著作用而活化。已知致癌基因v-Src會促進FAK的磷酸化作用,進一步改變細胞生長與形態特性。本篇利用FAK 基因剔除的老鼠胚胎纖維母細胞(FAK-/-),來研究FAK 在v-Src所導致的細胞轉形的過程中扮演的角色。實驗結果顯示,不論在in vitro或in vivo,FAK的表現會促進v-Src所造成的細胞轉形與腫瘤生成。在NIH 3T3/v-Src細胞中表現FAK-related non-kinase (FRNK),則能抑制v-Src所造成的細胞轉形與腫瘤生成。另外我們發現,誘發FAK Tyr-397突變株的表現,也會降低v-Src所造成細胞轉形與腫瘤生成。我們推測雖然FAK並非v-Src造成細胞轉形過程中,所絕對必須,但其表現可促進細胞轉形作用與腫瘤生成。

Focal adhesion kinase (FAK) is a nonreceptor protein-tyrosine kinase activated by tyrosine phosphorylation following integrin-mediated cell adhesion. The tyrosine phosphorylation of FAK enhanced by oncogenic Src has been proposed to contribute to altered cell growth and morphological properties associated with transformation. We utilized the fibroblasts derived from fak gene knockout mouse embryos to study the role of FAK in v-Src induced transformation. Overexpression of v-Src enhances phosphorylation level of FAK in cells. Results from focus formation assay and in vivo animal model suggested that FAK expression promotes v-Src-induced transformation and tumor growth. In addition, transient expression of FAK-related non-kinase (FRNK), which possesses dominant negative effect on FAK activity, suppressed v-Src-induced transformation and tumor growth. Remarkably, FAK Tyr397 mutant can decrease v-Src-induced transformation and tumor growth in nude mice. Taken together here we propose that although FAK is not essential for v-Src-induced transformation, it enhances v-Src-induced transformation and tumor growth.
Appears in Collections:生物化學研究所

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