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首页> 外文期刊>Cellular Physiology and Biochemistry >Tumor Cell-educated Periprostatic Adipose Tissue Acquires an Aggressive Cancer-promoting Secretory Profile
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Tumor Cell-educated Periprostatic Adipose Tissue Acquires an Aggressive Cancer-promoting Secretory Profile

机译：肿瘤细胞培养的前列腺癌脂肪组织获得了积极的促癌分泌谱

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Background/Aims The microenvironment produces important factors that are crucial to prostate cancer (PCa) progression. However, the extent to which the cancer cells stimulate periprostatic adipose tissue (PPAT) to produce these proteins is largely unknown. Our purpose was to determine whether PCa cell-derived factors influence PPAT metabolic activity. Methods Primary cultures of human PPAT samples from PCa patients (adipose tissue organotypic explants and primary stromal vascular fraction, SVF) were stimulated with conditioned medium (CM) collected from prostate carcinoma (PC3) cells. Cultures without CM were used as control. We used multiplex analysis and ELISA for protein quantification, qPCR to determine mitochondrial DNA (mtDNA) copy number and zymography for matrix metalloproteinase activity, in order to evaluate the response of adipose tissue explants and SVFs to PC3 CM. Results Stimulation of PPAT explants with PCa PC3 CM induced adipokines associated with cancer progression (osteopontin, tumoral necrosis factor alpha and interleukin-6) and reduced the expression of the protective adipokine adiponectin. Notably, osteopontin protein expression was 13-fold upregulated. Matrix metalloproteinase 9 activity and mitochondrial DNA copy number were higher after stimulation with cancer CM. Stromovascular cells from PPAT in culture were not influenced by tumor-derived factors. Conclusion The modulation of adipokine expression by tumor CM indicates the pervasive extent to which tumor cells command PPAT to produce factors favorable to their aggressiveness.
机译：背景/目的微环境产生对前列腺癌（PCa）进展至关重要的重要因素。但是，癌细胞刺激前列腺周围脂肪组织（PPAT）产生这些蛋白质的程度在很大程度上是未知的。我们的目的是确定PCa细胞衍生因子是否影响PPAT代谢活性。方法用从前列腺癌（PC3）细胞收集的条件培养基（CM）刺激PCa患者的人PPAT样品的原代培养物（脂肪组织器官外植体和原代基质血管部分，SVF）。没有CM的培养物用作对照。为了评估脂肪组织外植体和SVF对PC3 CM的反应，我们使用了多重分析和ELISA进行蛋白质定量，qPCR确定线粒体DNA（mtDNA）拷贝数和酶谱法测定基质金属蛋白酶活性。结果PCa PC3 CM刺激PPAT外植体诱导了与癌症进展相关的脂肪因子（骨桥蛋白，肿瘤坏死因子α和白介素6），并降低了保护性脂肪因子脂联素的表达。值得注意的是，骨桥蛋白的表达上调了13倍。癌症CM刺激后，基质金属蛋白酶9活性和线粒体DNA拷贝数较高。来自PPAT的培养的血管内皮细胞不受肿瘤来源因素的影响。结论肿瘤CM对脂肪因子表达的调节表明肿瘤细胞命令PPAT产生有利于其侵袭性的因子的普遍程度。

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