Coptisine induces G2/M arrest in esophageal cancer cell via the inhibition of p38/ERK1/2/claudin-2 signaling pathway
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.
Document Type: Research Article
Affiliations: 1: Laboratory of Immunology and Virology, Experiment Center for Science and Technology, Shanghai University of Traditional Chinese Medicine, Shanghai, China 2: Laboratory of Immunology and Virology, Experiment Center for Science and Technology, Shanghai University of Traditional Chinese Medicine, Shanghai, China;, Email: [email protected]
Publication date: 01 May 2021
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