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Tetrandrine Inhibits Epithelial-Mesenchymal Transition in IL-6-Induced HCT116 Human Colorectal Cancer Cells
OncoTargets and Therapy ( IF 2.7 ) Pub Date : 2021-08-21 , DOI: 10.2147/ott.s324552 Shih-Chang Tsai , Wei-Che Wu , Jai-Sing Yang
OncoTargets and Therapy ( IF 2.7 ) Pub Date : 2021-08-21 , DOI: 10.2147/ott.s324552 Shih-Chang Tsai , Wei-Che Wu , Jai-Sing Yang
Introduction: Patients with colorectal cancer (CRC) often develop distant metastases, which significantly reduces the 5-year survival rate. Epithelial-mesenchymal transition (EMT) is a crucial process for the invasion and metastasis of cancer cells. Tetrandrine has been reported to inhibit the viability and EMT of CRC cells; however, to the best of our knowledge, the molecular mechanism remains undetermined.
Methods: The MTT assay was used to determine HCT116 cell viability. Wound healing and Transwell assays were used to determine that cell migration and invasion, respectively. Western blotting analysis was performed to detect the expression of migration-related genes. Four different lengths of the E-cadherin gene promoter were constructed and cloned into pGL3 reporter plasmids to evaluate E-cadherin gene promoter activity.
Results: The results of the MTT assay revealed that tetrandrine inhibited HCT116 cell viability, with an IC50 value of 7.2 μM following 24 h of treatment. Tetrandrine inhibited IL-6-induced cell migration and invasion, respectively. Tetrandrine regulates the expression of migration-related genes in IL-6-stimulated HCT116 cells. Tetrandrine significantly downregulated the expression and enzyme activity of MMP-2 in IL-6-stimulated HCT116 cells. In addition, tetrandrine restored E-cadherin gene promoter activity.
Conclusion: The findings of the present study suggested that tetrandrine may inhibit EMT in IL-6-stimulated HCT116 cells; therefore, it may represent a potential drug for CRC.
Keywords: tetrandrine, IL-6, epithelial-mesenchymal transition, colorectal cancer
中文翻译：
粉防己碱抑制 IL-6 诱导的 HCT116 人结直肠癌细胞上皮间质转化
简介：结直肠癌 (CRC) 患者经常发生远处转移，这显着降低了 5 年生存率。上皮-间质转化（EMT）是癌细胞侵袭和转移的关键过程。据报道，粉防己碱可抑制 CRC 细胞的活力和 EMT；然而，据我们所知，分子机制仍未确定。
方法：MTT测定用于确定HCT116细胞活力。伤口愈合和 Transwell 测定分别用于确定细胞迁移和侵袭。进行蛋白质印迹分析以检测迁移相关基因的表达。构建了四种不同长度的 E-cadherin 基因启动子并将其克隆到 pGL3 报告质粒中以评估 E-cadherin 基因启动子活性。
结果： MTT 测定结果显示，汉防己碱抑制 HCT116 细胞活力，IC 50处理 24 小时后为 7.2 μM。粉防己碱分别抑制 IL-6 诱导的细胞迁移和侵袭。Tetrandrine 调节 IL-6 刺激的 HCT116 细胞中迁移相关基因的表达。粉防己碱显着下调 IL-6 刺激的 HCT116 细胞中 MMP-2 的表达和酶活性。此外，汉防己碱恢复了 E-cadherin 基因启动子的活性。
结论：本研究结果表明汉防己甲素可能抑制IL-6刺激的HCT116细胞的EMT；因此，它可能代表一种潜在的 CRC 药物。
关键词：汉防己素，IL-6，上皮-间质转化，结直肠癌
更新日期：2021-08-20
Methods: The MTT assay was used to determine HCT116 cell viability. Wound healing and Transwell assays were used to determine that cell migration and invasion, respectively. Western blotting analysis was performed to detect the expression of migration-related genes. Four different lengths of the E-cadherin gene promoter were constructed and cloned into pGL3 reporter plasmids to evaluate E-cadherin gene promoter activity.
Results: The results of the MTT assay revealed that tetrandrine inhibited HCT116 cell viability, with an IC50 value of 7.2 μM following 24 h of treatment. Tetrandrine inhibited IL-6-induced cell migration and invasion, respectively. Tetrandrine regulates the expression of migration-related genes in IL-6-stimulated HCT116 cells. Tetrandrine significantly downregulated the expression and enzyme activity of MMP-2 in IL-6-stimulated HCT116 cells. In addition, tetrandrine restored E-cadherin gene promoter activity.
Conclusion: The findings of the present study suggested that tetrandrine may inhibit EMT in IL-6-stimulated HCT116 cells; therefore, it may represent a potential drug for CRC.
Keywords: tetrandrine, IL-6, epithelial-mesenchymal transition, colorectal cancer
中文翻译：
粉防己碱抑制 IL-6 诱导的 HCT116 人结直肠癌细胞上皮间质转化
简介：结直肠癌 (CRC) 患者经常发生远处转移，这显着降低了 5 年生存率。上皮-间质转化（EMT）是癌细胞侵袭和转移的关键过程。据报道，粉防己碱可抑制 CRC 细胞的活力和 EMT；然而，据我们所知，分子机制仍未确定。
方法：MTT测定用于确定HCT116细胞活力。伤口愈合和 Transwell 测定分别用于确定细胞迁移和侵袭。进行蛋白质印迹分析以检测迁移相关基因的表达。构建了四种不同长度的 E-cadherin 基因启动子并将其克隆到 pGL3 报告质粒中以评估 E-cadherin 基因启动子活性。
结果： MTT 测定结果显示，汉防己碱抑制 HCT116 细胞活力，IC 50处理 24 小时后为 7.2 μM。粉防己碱分别抑制 IL-6 诱导的细胞迁移和侵袭。Tetrandrine 调节 IL-6 刺激的 HCT116 细胞中迁移相关基因的表达。粉防己碱显着下调 IL-6 刺激的 HCT116 细胞中 MMP-2 的表达和酶活性。此外，汉防己碱恢复了 E-cadherin 基因启动子的活性。
结论：本研究结果表明汉防己甲素可能抑制IL-6刺激的HCT116细胞的EMT；因此，它可能代表一种潜在的 CRC 药物。
关键词：汉防己素，IL-6，上皮-间质转化，结直肠癌
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