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首页> 外文期刊>Cell cycle >Focal adhesion kinase signaling and the aggressive melanoma phenotype.
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Focal adhesion kinase signaling and the aggressive melanoma phenotype.

机译：局灶性粘附激酶信号转导和侵袭性黑色素瘤表型。

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Focal adhesion kinase (FAK) mediates myriad cellular functions and has been found to be overexpressed in numerous human cancers. We recently explored the role of FAK in promoting the aggressive phenotype of melanoma cells, characterized by increased invasion, migration, and vasculogenic mimicry (VM) potential. We found FAK to be phosphorylated on its key tyrosine residues (397 and 576) in aggressive melanoma cells cultured on a three-dimensional type 1 collagen matrix in vitro, as well as in radial and vertical growth phase melanomas in situ. Furthermore, expressing FAK-related non-kinase (FRNK) in melanoma cells directly resulted in the inhibition of the aggressive phenotype, as demonstrated by decreased invasion, migration and VM potential, in part by blocking an Erk1/2 mediated signaling pathway. Additional data indicated that increased FAK activity may promote cellular proliferation and anchorage independent growth of aggressive melanoma. Together these observations implicate FAK as a promoter of the aggressive melanoma phenotype, thereby identifying a rational target for therapeutic intervention of malignant melanoma.
机译：黏着斑激酶（FAK）介导无数的细胞功能，并已发现在许多人类癌症中过表达。我们最近探讨了FAK在促进黑色素瘤细胞的侵袭性表型中的作用，其特征是增加了侵袭，迁移和血管生成模拟（VM）的潜力。我们发现，FAK在体外在三维1型胶原基质上培养的侵袭性黑素瘤细胞中以及在原位放射状和垂直生长期的黑素瘤中，其关键酪氨酸残基（397和576）被磷酸化。此外，在黑色素瘤细胞中表达FAK相关的非激酶（FRNK）直接导致了侵袭性表型的抑制，这通过减少的侵袭，迁移和VM电位证明，部分是通过阻断Erk1 / 2介导的信号传导途径来实现的。其他数据表明，增加的FAK活性可能促进侵袭性黑色素瘤的细胞增殖和锚定独立生长。这些观察结果共同暗示FAK是侵袭性黑素瘤表型的启动子，从而确定了恶性黑素瘤治疗干预的合理靶标。

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