肾母细胞瘤1蛋白和粘着斑激酶介导乳腺癌细胞中的角质形成细胞生长因子信号传导。
Wilms' tumor 1 protein and focal adhesion kinase mediate keratinocyte growth factor signaling in breast cancer cells.
作者信息
Zang Xiao-Ping, Pento J Thomas, Tari Ana M
机构信息
Department of Pharmaceutical Sciences, University of Oklahoma, Health Sciences Center, Oklahoma City, OK, USA.
出版信息
Anticancer Res. 2008 Jan-Feb;28(1A):133-7.
BACKGROUND
Keratinocyte growth factor (KGF) has been shown to induce breast cancer metastasis in animal models. cDNA microarrays have revealed that KGF increased Wilms tumor 1 (WT1) and focal adhesion kinase (FAK) expression in breast cancer cells. The role of WT1 and FAK in KGF signaling was investigated.
MATERIALS AND METHODS
A cell culture wounding model was used to study the effects of WT1 and FAK down-regulation on KGF-induced proliferation and motility in breast cancer cells.
RESULTS
WT1 down-regulation inhibited KGF-mediated proliferation and motility of breast cancer cells, while FAK down-regulation inhibited proliferation, but had no significant effect on cell motility. WT1 down-regulation, but not FAK down-regulation, led to Erk1,2 inactivation.
CONCLUSION
KGF-mediated signaling employs WT1 and FAK to regulate breast cancer cell proliferation and motility and may represent therapeutic targets for the prevention of breast cancer progression.
背景
在动物模型中，角质形成细胞生长因子（KGF）已被证明可诱导乳腺癌转移。cDNA微阵列显示，KGF可增加乳腺癌细胞中威尔姆斯瘤1（WT1）和粘着斑激酶（FAK）的表达。本研究调查了WT1和FAK在KGF信号传导中的作用。
材料与方法
采用细胞培养损伤模型，研究WT1和FAK下调对KGF诱导的乳腺癌细胞增殖和迁移的影响。
结果
WT1下调抑制了KGF介导的乳腺癌细胞增殖和迁移，而FAK下调抑制了增殖，但对细胞迁移无显著影响。WT1下调而非FAK下调导致Erk1,2失活。
结论
KGF介导的信号传导利用WT1和FAK来调节乳腺癌细胞的增殖和迁移，可能是预防乳腺癌进展的治疗靶点。
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