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Hydroxysafflor Yellow A of Carthamus Tinctorius L., Represses the Malignant Development of Esophageal Cancer Cells via Regulating NF-κB Signaling Pathway.
Cell Biochemistry and Biophysics ( IF 1.8 ) Pub Date : 2020-07-23 , DOI: 10.1007/s12013-020-00934-1
Xiumei Chen 1 , Yanfang Wang 2 , Lianjun Zhang 3 , Yujun Gao 4
Affiliation  

Esophageal cancer (EC) is a common digestive tract malignant tumor and the clinical outcome of patients with EC after surgery remains unsatisfactory. Hence, it is necessary to identify some effective drugs or methods to improve the prognosis of patients with EC. In this study, we attempted to analyze the potential role of hydroxysafflor yellow A (HSYA) in EC. Combined with The Cancer Genome Atlas (TCGA) and Comparative Toxicogenomics Database (CTD) as well as Database for Annotation, Visualization, and Integrated Discovery (DAVID) website, we tried to identify the related genes and pathways of HSYA. Then we estimated the actions of HSYA on proliferation, invasion and migration, and apoptosis of EC cells using cell counting kit 8, transwell and flow cytometry assays, respectively. At last, the expression of inflammatory protein and signaling pathway-related protein were measured using western blot analysis. Relative protein expression of intercellular adhesion molecule 1 (ICAM1), matrix metallopeptidase 9 (MMP9), tumor necrosis factor (TNF), and vascular cell adhesion molecule 1 (VCAM1) were all upregulated in EC tissues compared with normal tissues and they might be the target gene of HSYA according to bioinformatics analysis. HSYA exerted an inhibitory actions on cells proliferation, invasion, and migration but could accelerate the apoptosis of cells in EC. Moreover, HSYA could inhibit the expression of ICAM1, MMP9, TNF-α, and VCAM1 and induced the expression of phosphor-nuclear transcription factor kappa B p65 (p-P65) and phosphor-I kappa B-alpha (p-IκBα), but it did not influence the expression of P65 and IκBα. HSYA suppressed proliferation, invasion, and migration, simultaneously induce apoptosis of EC cells partly via regulating NF-κB signaling pathway.



中文翻译:


红花羟基红花黄 A 通过调节 NF-κB 信号通路抑制食管癌细胞的恶性发展。



食管癌(EC)是常见的消化道恶性肿瘤,食管癌患者术后临床预后仍不理想。因此,有必要寻找一些有效的药物或方法来改善EC患者的预后。在本研究中,我们试图分析羟基红花黄 A (HSYA) 在 EC 中的潜在作用。结合癌症基因组图谱(TCGA)和比较毒理学基因组数据库(CTD)以及注释、可视化和集成发现数据库(DAVID)网站,我们尝试鉴定HSYA的相关基因和通路。然后我们分别使用细胞计数试剂盒8、transwell和流式细胞术测定HSYA对EC细胞的增殖、侵袭和迁移以及凋亡的作用。最后,采用western blot分析检测炎症蛋白和信号通路相关蛋白的表达。与正常组织相比,EC 组织中细胞间粘附分子 1 (ICAM1)、基质金属肽酶 9 (MMP9)、肿瘤坏死因子 (TNF) 和血管细胞粘附分子 1 (VCAM1) 的相对蛋白表达均上调,可能是根据生物信息学分析HSYA的靶基因。 HSYA对EC细胞的增殖、侵袭和迁移有抑制作用,但可加速细胞凋亡。此外,HSYA 可抑制 ICAM1、MMP9、TNF-α 和 VCAM1 的表达,并诱导磷核转录因子 kappa B p65 (p-P65) 和磷-I kappa B-α (p-IκBα) 的表达。但不影响P65和IκBα的表达。 HSYA部分通过调节NF-κB信号通路抑制增殖、侵袭和迁移,同时诱导EC细胞凋亡。

更新日期:2020-07-23
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