Jia Yanmei, Chen Lirong, Guo Songjia, Li Yuanhong
Laboratory Medicine Department, Fenyang College, Shanxi Medical University, Fenyang, 032200, Shanxi, China.
Laboratory of Molecular Diagnosis and Treatment for Kidney Disease, Shanxi Provincial People's Hospital, Taiyuan, 030012, Shanxi, China.
Mol Biol Rep. 2019 Apr;46(2):1693-1700. doi: 10.1007/s11033-019-04618-9. Epub 2019 Feb 8.
To analyze the anti-tumor mechanism of Baicalin in human colon cancer. The MTT assay and colony formation assay demonstrated that Baicalin treatment inhibits the proliferation of DLD1 and HCT-116 cells. The apoptosis rates were induced upon Baicalin treatment and which was determined by FACS. The qPCR and western blot analysis showed that Baicalin promotes expression of DKK1 (Dickkopf), an important antagonist of Wnt signaling pathway, thereby reduces the expression of its downstream protein β-catenin and c-Myc. Reduction of DKK1 expression by siRNA attenuates β-catenin and c-Myc expression. microRNA-217 (miR-217) is decreased upon Baicalin treatment. Moreover, DKK1 is identified as the direct downstream target gene of miR-217 through the dual-luciferase reporter assay. miR-217/DKK1-mediated inhibition of Wnt signaling pathway participate in apoptosis induced by Baicalin.
为分析黄芩苷在人结肠癌中的抗肿瘤机制。MTT 法和集落形成试验表明，黄芩苷处理可抑制 DLD1 和 HCT-116 细胞的增殖。经黄芩苷处理后诱导了凋亡率，通过流式细胞术进行测定。qPCR 和蛋白质印迹分析表明，黄芩苷促进 Wnt 信号通路重要拮抗剂 DKK1（Dickkopf）的表达，从而降低其下游蛋白β-连环蛋白和 c-Myc 的表达。通过 siRNA 降低 DKK1 的表达可减弱β-连环蛋白和 c-Myc 的表达。黄芩苷处理后 microRNA-217（miR-217）降低。此外，通过双荧光素酶报告基因试验确定 DKK1 是 miR-217 的直接下游靶基因。miR-217/DKK1 介导的 Wnt 信号通路抑制参与了黄芩苷诱导的凋亡。
