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首页> 外文期刊>International journal of oncology >PRL-3 increases the aggressive phenotype of prostate cancer cells in vitro and its expression correlates with high-grade prostate tumors in patients
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PRL-3 increases the aggressive phenotype of prostate cancer cells in vitro and its expression correlates with high-grade prostate tumors in patients

机译：PRL-3在体外增加了前列腺癌细胞的侵袭性表型，其表达与患者的高度前列腺癌相关

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The increased expression of phosphatase of regenerating liver-3 (PRL-3) has been shown to be associated with the aggressive and metastatic phenotype of different solid tumors. However, it is not known whether PRL-3 plays a similar role in the progression of prostate cancer (PCa). In this study, immunoblot analysis of androgen receptor (AR)-positive PCa lines (LNCaP and LNCaP-SF) revealed the constitutive cytoplasmic expression of PRL-3, and stimulation with R1881 (AR agonist) rapidly increased the nuclear translocation of PRL-3. The AR-negative cell lines exhibited negligible PRL-3 expression, and the ectopic overexpression of PRL-3 increased both the proliferative and invasive potential of PC3 and DU145 cells. In addition, we measured PRL-3 protein expression in human prostate tumor sections. A high-density prostate tumor microarray (TMA) was immunostained to assess whether PRL-3 expression and its subcellular localization (cytoplasmic and nuclear levels) is associated with the Gleason score (GS), Gleason grade (GG) and tumor stage (T-stage). Digital image analysis (DIA) revealed that PRL-3 expression was significantly higher in the malignant cores, as compared to the non-malignant areas. Increases in both total and nuclear PRL-3 levels were also associated with a higher GS and GG. Metastatic tumors (T4-stage) had lower cytoplasmic, but higher nuclear PRL-3 levels. Furthermore, the nuclear/cytoplasmic ratio for PRL-3 in the tumors graded as GS7 could effectively distinguish between indolent (3+4) and aggressive (4+3) disease. Thus, our experiments using PCa lines suggested that PRL-3 is an AR-regulated gene and its androgen-induced nuclear localization may increase the aggressive behavior of PCa cells. Furthermore, the digital analysis of immunostained tumor sections suggested that PRL-3 may be an effective biomarker of high-grade PCa, and its nuclear/cytoplasmic ratio may be used to distinguish between indolent vs. aggressive tumors.
机译：已显示再生肝3（PRL-3）磷酸酶表达的增加与不同实体瘤的侵袭性和转移表型有关。然而，还不知道PRL-3在前列腺癌（PCa）的进展中是否起类似的作用。在这项研究中，雄激素受体（AR）阳性PCa系（LNCaP和LNCaP-SF）的免疫印迹分析揭示了PRL-3的组成型细胞质表达，并且用R1881（AR激动剂）刺激迅速增加了PRL-3的核转运。 AR阴性细胞系的PRL-3表达可忽略不计，而异位表达PRL-3可增加PC3和DU145细胞的增殖和侵袭能力。此外，我们测量了人类前列腺肿瘤切片中的PRL-3蛋白表达。对高密度前列腺肿瘤微阵列（TMA）进行了免疫染色，以评估PRL-3的表达及其亚细胞定位（细胞质和细胞核水平）是否与格里森评分（GS），格里森分级（GG）和肿瘤分期（T-阶段）。数字图像分析（DIA）显示，与非恶性区域相比，PRL-3表达在恶性核中显着更高。总PRL-3和核PRL-3水平的增加也与较高的GS和GG有关。转移性肿瘤（T4期）细胞质较低，但核PRL-3水平较高。此外，分级为GS7的肿瘤中PRL-3的核/细胞质比率可以有效地区分惰性疾病（3 + 4）和侵袭性疾病（4 + 3）。因此，我们使用PCa细胞系的实验表明PRL-3是AR调控的基因，其雄激素诱导的核定位可能会增加PCa细胞的侵袭性。此外，对免疫染色肿瘤切片的数字分析表明，PRL-3可能是高级PCa的有效生物标志物，其核/胞质比可用于区分惰性肿瘤与侵袭性肿瘤。

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