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人前列腺周围脂肪组织:其对前列腺癌细胞的影响。

Human periprostatic adipose tissue: its influence on prostate cancer cells.

作者信息

Sacca Paula Alejandra, Creydt Virginia Pistone, Choi Hosoon, Mazza Osvaldo Néstor, Fletcher Sabrina Johanna, Vallone Valeria Beatriz Fernández, Scorticati Carlos, Chasseing Norma Alejandra, Calvo Juan Carlos

机构信息

Instituto de Biología y Medicina Experimental (IBYME)-CONICET, Buenos Aires, Argentina.

出版信息

Cell Physiol Biochem. 2012;30(1):113-22. doi: 10.1159/000339051. Epub 2012 Jun 13.

Abstract

BACKGROUND/AIMS: Adipose microenvironment is involved in signaling pathways that influence prostate cancer (PCa) progression. However, the role of human periprostatic adipose tissue (PPAT) from patients with benign prostatic hyperplasia (BPH) has not been studied and compared to that of PPAT from PCa patients. The aim of this paper was to investigate the influence of factors derived from both PPATs on the behavior of androgen-dependent and castration resistant PCa cells.

METHODS

PPAT conditioned media (CM) were obtained from tissue samples from patients with clinically primary PCa (TPPAT) or BPH (BPPAT). Cell adhesion, proliferation, migration and metalloproteinase expression were evaluated following exposure of LNCaP (androgen dependent) and PC3 (androgen independent) prostate cancer cell lines to BPPAT or TPPAT CM.

RESULTS

Proliferation or motility of LNCaP or PC3 cells were not significantly affected by TPPAT or BPPAT CM. The number of LNCaP but not PC3 cells attached to components of TPPAT CM significantly decreased compared to cells attached to BPPAT CM. PPAT produced and released pro-MMP-9. Zymograms demonstrated that TPPAT CM induced a significant increase in pro-MMP-9 activity compared to BPPAT CM in LNCaP cells but not in PC3 cells.

CONCLUSIONS

We conclude that TPPAT released factors, such as pro-MMP-9, could induce the invasive capacity of LNCaP cells and speculate that PPAT derived factors could, in the early stages of prostate cancer, modulate disease progression.

摘要

背景/目的:脂肪微环境参与影响前列腺癌(PCa)进展的信号通路。然而,来自良性前列腺增生(BPH)患者的人前列腺周围脂肪组织(PPAT)的作用尚未得到研究,也未与来自PCa患者的PPAT进行比较。本文的目的是研究来自两种PPAT的因子对雄激素依赖性和去势抵抗性PCa细胞行为的影响。

方法

从临床原发性PCa患者(TPPAT)或BPH患者(BPPAT)的组织样本中获得PPAT条件培养基(CM)。将LNCaP(雄激素依赖性)和PC3(雄激素非依赖性)前列腺癌细胞系暴露于BPPAT或TPPAT CM后,评估细胞粘附、增殖、迁移和金属蛋白酶表达。

结果

TPPAT或BPPAT CM对LNCaP或PC3细胞的增殖或运动性无显著影响。与附着于BPPAT CM的细胞相比,附着于TPPAT CM成分的LNCaP细胞数量显著减少,但PC3细胞数量未减少。PPAT产生并释放前基质金属蛋白酶-9(pro-MMP-9)。酶谱分析表明,与BPPAT CM相比,TPPAT CM在LNCaP细胞中诱导pro-MMP-9活性显著增加,但在PC3细胞中未增加。

结论

我们得出结论,TPPAT释放的因子,如pro-MMP-9,可诱导LNCaP细胞的侵袭能力,并推测PPAT衍生的因子可能在前列腺癌的早期阶段调节疾病进展。

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