小檗碱通过抑制 p38/ERK1/2/闭合蛋白-2 信号通路诱导食管癌 G2/M 期阻滞。
Coptisine induces G2/M arrest in esophageal cancer cell via the inhibition of p38/ERK1/2/claudin-2 signaling pathway.
机构信息
Laboratory of Immunology and Virology, Experiment Center for Science and Technology, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Laboratory of Immunology and Virology, Experiment Center for Science and Technology, Shanghai University of Traditional Chinese Medicine, Shanghai, China;, Email:
出版信息
Pharmazie. 2021 May 1;76(5):202-207. doi: 10.1691/ph.2021.1353.
In this study, we treated esophageal cancer (EC) cell lines, TE1 and KYSE450 with coptisine (COP) and investigated the biological effects of COP in EC cells. Our results showed that COP inhibited the cell viability and proliferation of EC cells, and COP induced G2/M phase arrest of EC cells and decreased the expression of claudin-2, p-cdc2, CDK1 and cyclin B1. In addition, we found the reduction of p-p38 and p-ERK1/2 in EC cells treated with COP. The effects of COP on pro-cell cycle arresting were reversed after combined with p38 and ERK1/2 inhibitors. Overall, these findings indicate that COP may possess potential for anti-tumor effects in EC and may contribute to the development as anti-cancer agents.
在这项研究中，我们用黄连碱（COP）处理食管癌细胞系 TE1 和 KYSE450，并研究了 COP 对食管癌细胞的生物学效应。结果表明，COP 抑制了食管癌细胞的活力和增殖，COP 诱导食管癌细胞 G2/M 期阻滞，并降低了 Claudin-2、p-cdc2、CDK1 和 cyclin B1 的表达。此外，我们发现 COP 处理后的食管癌细胞中 p-p38 和 p-ERK1/2 的表达减少。用 p38 和 ERK1/2 抑制剂处理后，COP 对细胞周期阻滞的作用得到逆转。总的来说，这些发现表明 COP 可能具有在食管癌中抗肿瘤作用的潜力，并可能有助于开发抗癌药物。
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