Xia Wang1, Yang Zhang2, Shiyu Zhang2, Liangwei Duan3. 1. College of Life Sciences, Nankai University, Tianjin, 300071, China. 2. Henan Key Laboratory of Immunology and Targeted Drugs, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, 453003, Henan, China. 3. Henan Key Laboratory of Immunology and Targeted Drugs, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, 453003, Henan, China. Electronic address: duanliangwei666@hotmail.com.
Abstract
OBJECTIVE: The aim of this study was to investigate the role and molecular regulatory mechanisms of baicalin in oral squamous cell carcinoma (OSCC) progression. DESIGN: Gene expression in OSCC cells was detected by quantitative reverse transcription polymerase chain reaction (RT-qPCR). OSCC cell viability, migration, invasion and stemness were measured by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), 5-ethynyl-2'-deoxyuridine (EdU), wound healing, Transwell, and sphere formation assays. The target genes of miR-106b-5p were predicted using bioinformatic tools. The interaction between microRNA-miR-106b-5p (miR-106b-5p) and disabled homolog 2 (DAB2) was confirmed by a luciferase reporter assay. TOP/FOP-Flash reporter assay and western blot analysis were used to analyze the activity of the Wnt/β-catenin pathway. RESULTS: Baicalin inhibited OSCC cell viability, migration, invasion, and stemness. Baicalin downregulated miR-106b-5p expression. In addition, MiR-106b-5p upregulation reversed the effects of baicalin on OSCC cells. As a target gene of miR-106b-5p, DAB2 was negatively regulated by miR-106b-5p and upregulated by baicalin in OSCC cells. MiR-106b-5p activated Wnt/β-catenin pathway in OSCC cells by inhibiting DAB2. Baicalin suppressed Wnt/β-catenin pathway by upregulating DAB2. In rescue assays, miR-106b-5p overexpression-induced promotion of OSCC cellular processes was attenuated by DAB2 upregulation. CONCLUSIONS: Baicalin exerts anti-tumor effects in OSCC by inhibiting the miR-106b-5p-Wnt/β-catenin pathway via upregulating DAB2.
OBJECTIVE: The aim of this study was to investigate the role and molecular regulatory mechanisms of baicalin in oral squamous cell carcinoma (OSCC) progression. DESIGN: Gene expression in OSCC cells was detected by quantitative reverse transcription polymerase chain reaction (RT-qPCR). OSCC cell viability, migration, invasion and stemness were measured by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), 5-ethynyl-2'-deoxyuridine (EdU), wound healing, Transwell, and sphere formation assays. The target genes of miR-106b-5p were predicted using bioinformatic tools. The interaction between microRNA-miR-106b-5p (miR-106b-5p) and disabled homolog 2 (DAB2) was confirmed by a luciferase reporter assay. TOP/FOP-Flash reporter assay and western blot analysis were used to analyze the activity of the Wnt/β-catenin pathway. RESULTS: Baicalin inhibited OSCC cell viability, migration, invasion, and stemness. Baicalin downregulated miR-106b-5p expression. In addition, MiR-106b-5p upregulation reversed the effects of baicalin on OSCC cells. As a target gene of miR-106b-5p, DAB2 was negatively regulated by miR-106b-5p and upregulated by baicalin in OSCC cells. MiR-106b-5p activated Wnt/β-catenin pathway in OSCC cells by inhibiting DAB2. Baicalin suppressed Wnt/β-catenin pathway by upregulating DAB2. In rescue assays, miR-106b-5p overexpression-induced promotion of OSCC cellular processes was attenuated by DAB2 upregulation. CONCLUSIONS: Baicalin exerts anti-tumor effects in OSCC by inhibiting the miR-106b-5p-Wnt/β-catenin pathway via upregulating DAB2.