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Article Publish Status: FREE
Abstract Title:

Ginsenoside compound K inhibits nuclear factor-kappa B by targeting Annexin A2.

Abstract Source:

J Ginseng Res. 2019 Jul ;43(3):452-459. Epub 2018 Apr 21. PMID: 31308817

Abstract Author(s):

Yu-Shi Wang, Hongyan Zhu, He Li, Yang Li, Bing Zhao, Ying-Hua Jin

Article Affiliation:

Yu-Shi Wang

Abstract:

Background: Ginsenoside compound K(C-K), a major metabolite of ginsenoside, exhibits anticancer activity in various cancer cells and animal models. A cell signaling study has shown that C-K inhibited nuclear factor-kappa B (NF-κB) pathway in human astroglial cells and liver cancer cells. However, the molecular targets of C-K and the initiating events were not elucidated.

Methods: Interaction between C-K and Annexin A2 was determined by molecular docking and thermal shift assay. HepG2 cells were treated with C-K, followed by a luciferase reporter assay for NF-кB, immunofluorescence imaging for the subcellular localization of Annexin A2 and NF-кB p50 subunit, coimmunoprecipitation of Annexin A2 and NF-кB p50 subunit, and both cell viability assay and plate clone formation assay to determine the cell viability.

Results: Both molecular docking and thermal shift assay positively confirmed the interaction between Annexin A2 and C-K. This interaction prevented the interaction between Annexin A2 and NF-кB p50 subunit and their nuclear colocalization, which attenuated the activation of NF-кB and the expression of its downstream genes, followed by the activation of caspase 9 and 3. In addition, the overexpression of Annexin A2-K320A, a C-K binding-deficient mutant of Annexin A2, rendered cells toresist C-K treatment, indicating that C-K exerts its cytotoxic activity mainly by targeting Annexin A2.

Conclusion: This study for the first time revealed a cellular target of C-K and the molecular mechanism for its anticancer activity.

Study Type : In Vitro Study

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Sayer Ji
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