目的:Alisol A是从泽泻中分离得到的具有生物活性的三萜类化合物,具有抗癌潜能。本研究旨在探讨Alisol A对鼻咽癌细胞生长的影响。方法:MTT实验、集落形成实验、流式细胞术、transwell实验、伤口愈合实验分别检测细胞活力、增殖、细胞周期、迁移、侵袭。结果:Alisol A可抑制鼻咽癌细胞的活力、增殖、迁移和侵袭。Alisol A对C666-1和HK1细胞的生长有明显的抑制作用,并呈时间和浓度依赖性。Alisol A处理显著降低了鼻咽癌细胞中细胞周期相关基因的蛋白表达。在Alisol A处理的细胞中,鼻咽癌细胞的迁移和侵袭能力降低。Alisol A处理显著降低了鼻咽癌细胞中MMP2和MMP9的蛋白表达。结论:Alisol A抑制鼻咽癌细胞的增殖、迁移和侵袭。Alisol A可能是治疗鼻咽癌的靶点。Purpose: Alisol A is a bioactive triterpenoid isolated from the Rhizoma alismatis, which has anticancer potential. In this study, we explored the effect of Alisol A on the growth of nasopharyngeal carcinoma (NPC) cells. Methods: MTT assay, colony formation assay, flow cytometry, transwell assay, wound healing assay were used to assess cell viability, proliferation, cell cycle, migration, invasion, respectively, in vitro. Results: Alisol A inhibited the viability, proliferation, migration, and invasion of NPC cells. Alisol A significantly inhibited the growth of C666-1 and HK1 cells in a time- and concentration-dependent manner. Alisol A treatment significantly reduced the protein expression of cell cycle-related genes in NPC cells. The migration and invasion abilities of NPC cells were reduced in Alisol A-treated cells. Alisol A treatment significantly reduced the protein expression of MMP2 and MMP9 in NPC cells. Conclusion: Alisol A inhibited the proliferation, migration, and invasion of NPC cells. Alisol A may be a potential therapeutic target for nasopharyngeal.
背景:鼻咽癌(Nasopharyngeal carcinoma, NPC)是一种源于鼻咽上皮的恶性肿瘤。Alisol A是一种来源于泽泻根茎的三萜类化合物,具有抑制癌细胞生长和诱导癌细胞凋亡的能力。Alisol A对鼻咽癌的影响尚不明确。方法:Western blot检测蛋白表达。采用AutoDock Vina和Discovery Studio软件进行分子对接。结果:Alisol A可抑制鼻咽癌细胞的活力、增殖、迁移和侵袭。分子对接模拟实验证实Alisol A与YAP蛋白结合。此外,在鼻咽癌细胞中,Alisol A促进YAP的磷酸化并抑制YAP的表达。结论:Alisol A通过抑制Hippo信号通路抑制鼻咽癌细胞。Alisol A可能是治疗鼻咽癌的候选药物。Background: Nasopharyngeal carcinoma (NPC) is a malignant tumor originating from the nasopharyngeal epithelium. Alisol A, a triterpenoid compound derived from rhizome of Alismatis alismatis, has been shown to inhibit cancer cell growth and induce apoptosis. The effect of Alisol A on nasopharyngeal carcinoma (NPC) is still unclear. Methods: Western blot was used to detect protein expression. AutoDock Vina and Discovery Studio software were used for molecular docking. Results: Alisol A inhibited the viability, proliferation, migration, and invasion of NPC cells. The molecular docking simulation assay confirmed that Alisol A is bound to YAP protein. In addition, Alisol A promoted the phosphorylation of YAP and suppressed the expression of YAP in NPC cells. Conclusion: Alisol A inhibits the growth of NPC cells by inhibiting Hippo signaling pathway. Alisol A may be a candidate drug for the treatment of NPC.
