FYN is overexpressed in human prostate cancer.
FYN is overexpressed in human prostate cancer.
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DOI：
10.1111/j.1464-410x.2008.08009.x
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发表时间：
2009-01
影响因子：
4.5
通讯作者：
Salgia R
中科院分区：
文献类型：
--
作者：
Posadas EM;Al-Ahmadie H;Robinson VL;Jagadeeswaran R;Otto K;Kasza KE;Tretiakov M;Siddiqui J;Pienta KJ;Stadler WM;Rinker-Schaeffer C;Salgia R
FYN是SRC激酶家族（SFK）的成员，在功能上与其他SFK不同。它与FAK和桩蛋白（PXN）-细胞形态和运动的调节剂相互作用。我们假设FYN在前列腺癌（CaP）中上调。Oncomine中的数据挖掘免疫印迹和定量RT-PCR和免疫组化分析的细胞系分析，我们描述了FYN在CaP中的表达。该分析包括32例CaP，9例前列腺上皮内瘤变（PIN）和19例正常。对样本的染色腺体百分比和染色强度（0-3）进行评分。每个样本都被分配了一个由百分比和强度相乘产生的综合评分。数据挖掘显示，与正常组织相比，CaP中的FYN表达增加了8倍。这是FYN特有的，其他SFK不存在。采用定量RT-PCR和免疫印迹法检测FYN在CaP细胞系（LNCaP、22 Rv 1、PC 3、DuPro）中的表达。FYN及其信号伴侣FAK和PXN的表达在人体组织中得到证实。与正常人相比，FYN的中位综合评分增加了2.1倍（p<0.001），FAK增加了1.7倍（p<0.001），PXN增加了2倍（p<0.05）。与PIN相比，CaP中FYN增加1.7倍（p<0.05），FAK增加1.6倍（p<0.01）。这些研究支持FYN及其相关信号传导伙伴在CaP中上调的假设，并支持进一步研究FYN作为治疗靶点的作用。
FYN is a member of the SRC family of kinases (SFKs), functionally distinct from other SFKs. It interacts with FAK and paxillin (PXN)- regulators of cell morphology and motility. We hypothesized that FYN is upregulated in prostate cancer (CaP). Through datamining in Oncomine; cell line profiling with immunoblotting and quantitative RT-PCR; and immunohistochemical analysis, we describe FYN expression in CaP. This analysis included 32 cases of CaP, 9 prostatic intraepithelial neoplasia (PIN), and 19 normal. Samples were scored for the percentage of stained glands and intensity of staining (from 0-3). Each sample was assigned a composite score generated by multiplying percentage and intensity. Datamining showed an 8-fold increase in FYN expression in CaP compared to normal tissue. This was specific to FYN and not present for other SFKs. Expression of FYN in CaP cell lines (LNCaP, 22Rv1, PC3, DuPro) was detected using quantitative RT-PCR and immunoblot. Expression of FYN and its signaling partners FAK and PXN was demonstrated in human tissue. Comparing normal to cancer, there was a 2.1-fold increase in median composite score for FYN (p<0.001) 1.7-fold increase in FAK (p<0.001), and a 2-fold increase in PXN (p<0.05). There was a 1.7-fold increase in FYN (p<0.05), a 1.6-fold increase in FAK (p<0.01) in CaP as compared to PIN. These studies support the hypothesis that the FYN and its related signaling partners are upregulated in CaP and supports further investigation into the role of the FYN as a therapeutic target.