Tumor formation of prostate cancer cells influenced by stromal cells from the transitional or peripheral zones of the normal prostate.
Tumor formation of prostate cancer cells influenced by stromal cells from the transitional or peripheral zones of the normal prostate.
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DOI：
10.1038/aja.2008.33
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发表时间：
2009-01
影响因子：
2.9
通讯作者：
Fu-jun Zhao;B. Han;Sheng-qiang Yu;S. Xia
中科院分区：
文献类型：
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作者：
Fu-jun Zhao;B. Han;Sheng-qiang Yu;S. Xia
本研究旨在通过体外和体内共培养模型，探讨前列腺移行区（TZ）和外周区（PZ）基质细胞在前列腺癌（PC a）上皮细胞（PC-3）癌变过程中的不同参与。应用电镜和基因芯片技术对原代培养的人前列腺TZ和PZ间质细胞的超微结构和基因表达谱进行分析。建立了正常TZ或PZ基质细胞与人前列腺癌PC-3细胞的体外和体内共培养模型。我们在体内裸鼠模型中评估肿瘤生长和重量。正常前列腺TZ和PZ间质细胞在形态和超微结构上存在差异。在所有的，514差异表达基因的芯片分析，选择483个基因更高的表达在基质细胞从TZ和31个更高的表达在那些从PZ。PZ基质细胞与转化生长因子-β1（transforming growth factor-β 1，TGF-β1）共培养可促进PC-3细胞的体内外肿瘤生长，并促进Bcl-2的表达。另一方面，TZ的基质细胞抑制小鼠模型中PC-3细胞肿瘤的生长。我们的结论是，超微结构和基因表达之间的基质细胞从TZ或PZ的正常前列腺，和TZ或PZ的基质-上皮细胞的相互作用可能是负责不同的区域定位的前列腺肿瘤形成。
This study was designed to investigate the different involvements of prostatic stromal cells from the normal transitional zone (TZ) or peripheral zone (PZ) in the carcinogenesis of prostate cancer (PCa) epithelial cells (PC-3) in vitro and in vivo co-culture models. Ultra-structures and gene expression profiles of primary cultures of human prostatic stromal cells from the normal TZ or PZ were analyzed by electron microscopy and microarray analysis. In vitro and in vivo co-culture models composed of normal TZ or PZ stromal cells and human PCa PC-3 cells were established. We assessed tumor growth and weight in the in vivo nude mice model. There are morphological and ultra-structural differences in stromal cells from TZ and PZ of the normal prostate. In all, 514 differentially expressed genes were selected by microarray analysis; 483 genes were more highly expressed in stromal cells from TZ and 31 were more highly expressed in those from PZ. Co-culture with PZ stromal cells and transforming growth factor-β1 (TGF-β1) increased the tumor growth of PC-3 cells in vitro and in vivo, as well as Bcl-2 expression. On the other hand, stromal cells of TZ suppressed PC-3 cell tumor growth in the mouse model. We conclude that ultra-structures and gene expression differ between the stromal cells from TZ or PZ of the normal prostate, and stroma–epithelium interactions from TZ or PZ might be responsible for the distinct zonal localization of prostate tumor formation.