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首页> 美国卫生研究院文献>Scientific Reports >NES1/KLK10 gene represses proliferation enhances apoptosis and down-regulates glucose metabolism of PC3 prostate cancer cells
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NES1/KLK10 gene represses proliferation enhances apoptosis and down-regulates glucose metabolism of PC3 prostate cancer cells

机译：NES1 / KLK10基因抑制PC3前列腺癌细胞的增殖增强细胞凋亡并下调葡萄糖代谢

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The normal epithelial cell-specific-1 (NES1) gene, also named as KLK10, is recognised as a novel putative tumour suppressor in breast cancer, but few studies have focused on the function of KLK10 in human prostate cancer. Our study confirms that the expression of KLK10 in prostate cancer tissue and cell lines (PC3, DU145, and LNCaP clone FGC) is low. Given that the androgen-independent growth characteristic of the PC3 cell line is more similar to clinical castration-resistant prostate cancer, we studied the role of KLK10 in PC3. In vitro and in vivo assays showed that over-expressing KLK10 in PC3 could decelerate tumour proliferation, which was accompanied with an increase in apoptosis and suppression of glucose metabolism. The related proteins, such as Bcl-2 and HK-2, were down-regulated subsequently. Furthermore, by up-regulating Bcl-2 or HK-2 respectively in the PC3-KLK10 cell line, we observed a subsequent increase of cell proliferation and a synchronous up-regulation of HK-2 and Bcl-2. Besides, KLK10 expression was also increased by Bcl-2 and HK-2, which suggests that there is a negative feedback loop between KLK10 and Bcl-2/HK-2. Thus, our results demonstrated that KLK10 may function as a tumour suppressor by repressing proliferation, enhancing apoptosis and decreasing glucose metabolism in PC3 cells.
机译：正常上皮细胞特异性-1（NES1）基因，也称为KLK10，被公认为是乳腺癌中一种新型的假定肿瘤抑制因子，但是很少有研究集中于KLK10在人前列腺癌中的功能。我们的研究证实，KLK10在前列腺癌组织和细胞系（PC3，DU145和LNCaP克隆FGC）中的表达较低。考虑到PC3细胞系的雄激素非依赖性生长特征与临床去势抵抗性前列腺癌更为相似，我们研究了KLK10在PC3中的作用。体外和体内试验表明，在PC3中过表达KLK10可以减缓肿瘤的增殖，并伴随凋亡增加和葡萄糖代谢的抑制。随后下调了相关蛋白，例如Bcl-2和HK-2。此外，通过分别上调PC3-KLK10细胞系中的Bcl-2或HK-2，我们观察到随后细胞增殖增加以及HK-2和Bcl-2同步上调。此外，Bcl-2和HK-2也增加了KLK10的表达，这提示KLK10与Bcl-2 / HK-2之间存在负反馈回路。因此，我们的结果表明，KLK10可以通过抑制PC3细胞中的增殖，增强细胞凋亡和减少葡萄糖代谢来起到抑癌作用。

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