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首页> 外文期刊>Cell biology international. >Calprotectin induces cell death in human prostate cancer cell (LNCaP) through survivin protein alteration
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Calprotectin induces cell death in human prostate cancer cell (LNCaP) through survivin protein alteration

机译：钙卫蛋白通过生存素蛋白改变诱导人前列腺癌细胞（LNCaP）细胞死亡

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摘要

Calprotectin (CP), an abundant heterodimeric cytosolic protein of neutrophils, conveys a variety of functions such as tumor cell growth arrest and antimicrobial activity. We investigated CP activity and its possible apoptosis-inducing mechanism of action against an antiandrogen therapy-resistance prostate cancer cell line LNCaP. Cell viability and Annexin V FITC assays were performed in order to investigate its cell death activity and apoptosis, respectively. In order to address cell death inducing mechanism(s), immunocytochemistry and immunobloting analysis, reactive oxygen species (ROS) and nitric oxide (NO) measurements were performed. The effective concentration of CP against LNCaP promoting LNCaP cell death was 200 μg/mL. ROS and NO levels of cells remarkably were enhanced following treatment with 50 and 100μg/mL of CP, respectively. Protein expression of anti-apoptotic protein survivin was significantly decreased after administration of tumor cells with CP. Our data indicate that CP regulates the LNCaP cells viability via survivin-mediated pathway and ROS and NO enhancement. Thus, inhibition of survivin expression, enhancement of ROS and NO level by CP or other similar pharmaceutical agents might be effective in lowering the malignant proliferation of human prostate cancer cells.
机译：钙卫蛋白（CP）是嗜中性粒细胞中丰富的异源二聚体胞质蛋白，具有多种功能，例如阻止肿瘤细胞的生长和抗菌活性。我们调查了CP活性及其对抗雄激素治疗耐药性前列腺癌细胞系LNCaP的可能的凋亡诱导作用机制。进行细胞存活力和膜联蛋白V FITC测定以分别研究其细胞死亡活性和细胞凋亡。为了解决诱导细胞死亡的机制，免疫细胞化学和免疫印迹分析，活性氧（ROS）和一氧化氮（NO）的测量方法。抗LNCaP促进LNCaP细胞死亡的CP的有效浓度为200μg/ mL。分别用50和100μg/ mL的CP处理后，细胞的ROS和NO水平显着提高。用CP施用肿瘤细胞后，抗凋亡蛋白survivin的蛋白表达显着降低。我们的数据表明CP通过Survivin介导的途径以及ROS和NO的增强来调节LNCaP细胞的活力。因此，CP或其他类似药物对survivin表达的抑制，ROS和NO水平的增强可能在降低人前列腺癌细胞的恶性增殖方面是有效的。

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