Nanotechnology is a developing and revolutionary science that has been widely recommended for diagnosis and treatment of cancer. Among the various nanoparticles used in nanotechnology, gold nanoparticles (AuNPs) have attracted much attentions due to their promising anticancer properties. Despite the potential advantages of AuNPs, their apoptotic and anti-angiogenic effects have not yet been reported on human bladder cancer 5637 cells. This motivated us to evaluate (reactive oxygen species) ROS-mediated apoptosis in 5637 cells. For this task, inhibitory effect of AuNPs was investigated after 24-h exposure to different concentrations of AuNPs by MTT assay. Also, apoptosis level was assessed by ROS production, flow cytometry, and Hoechst 33,258 staining. Besides, mRNA expression of B-cell lymphoma protein 2 (Bcl-2), Bcl-2-associated X (Bax), vascular endothelial growth factor A (VEGFA) genes, and caspase-3,7 activity were determined by qRT-PCR and colorimetric assay, respectively. Moreover, migration rate was evaluated by wound healing assay. MTT results demonstrate that AuNPs can reduce 5637-cell viability in a dose-dependent manner, while fluorimetric assay data show significant increased ROS production in 25 and 50 µg/ml-treated cells. It is also observed that AuNPs lead to Bax overexpression and downregulation of Bcl-2 and VEGFA genes. In line with this, flow cytometry results show increased levels of apoptosis in 25 and 50 µg/ml AuNP-treated cells (p < 0.05). Similarly, Hoechst staining indicates a remarkable increase in cells with apoptotic morphology after treating with AuNPs. Overall, our findings show that AuNPs significantly provoke ROS production, induce apoptosis, and suppress cell migration in bladder cancer 5637 cells.

纳米技术是一门发展中的革命性科学，已被广泛推荐用于癌症的诊断和治疗。在纳米技术中使用的各种纳米粒子中，金纳米粒子（AuNPs）因其具有良好的抗癌特性而备受关注。尽管金纳米粒子具有潜在的优势，但其对人膀胱癌 5637 细胞的凋亡和抗血管生成作用尚未见报道。这促使我们在 5637 细胞中评估（活性氧）ROS 介导的细胞凋亡。对于这项任务，通过 MTT 测定法在暴露于不同浓度的 AuNPs 24 小时后研究了 AuNPs 的抑制作用。此外，通过 ROS 产生、流式细胞术和 Hoechst 33,258 染色评估细胞凋亡水平。此外，B 细胞淋巴瘤蛋白 2 (Bcl-2)、Bcl-2 相关 X (Bax)、血管内皮生长因子 A (VEGFA) 基因和 caspase-3,7 活性分别通过 qRT-PCR 和比色法测定。此外，通过伤口愈合试验评估迁移率。MTT 结果表明，AuNPs 可以以剂量依赖性方式降低 5637 细胞的活力，而荧光测定数据显示 25 和 50 µg/ml 处理的细胞中 ROS 的产生显着增加。还观察到 AuNPs 导致 Bax 过表达和 Bcl-2 和 VEGFA 基因的下调。与此一致，流式细胞术结果显示 25 和 50 µg/ml AuNP 处理的细胞凋亡水平增加（MTT 结果表明，AuNPs 可以以剂量依赖性方式降低 5637 细胞的活力，而荧光测定数据显示 25 和 50 µg/ml 处理的细胞中 ROS 的产生显着增加。还观察到 AuNPs 导致 Bax 过表达和 Bcl-2 和 VEGFA 基因的下调。与此一致，流式细胞术结果显示 25 和 50 µg/ml AuNP 处理的细胞凋亡水平增加（MTT 结果表明，AuNPs 可以以剂量依赖性方式降低 5637 细胞的活力，而荧光测定数据显示 25 和 50 µg/ml 处理的细胞中 ROS 的产生显着增加。还观察到 AuNPs 导致 Bax 过表达和 Bcl-2 和 VEGFA 基因的下调。与此一致，流式细胞术结果显示 25 和 50 µg/ml AuNP 处理的细胞凋亡水平增加（p  < 0.05)。类似地，Hoechst 染色表明用 AuNPs 处理后具有凋亡形态的细胞显着增加。总体而言，我们的研究结果表明，AuNPs 在膀胱癌 5637 细胞中显着激发 ROS 产生、诱导细胞凋亡并抑制细胞迁移。