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CJAP ›› 2019, Vol. 35 ›› Issue (5): 428-432.doi: 10.12047/j.cjap.5809.2019.093

• ORIGINAL ARTICLES • Previous Articles     Next Articles

Effects of dihydromyricetin on the migration and invasion of human gastric cancer MKN45 cells and its mechanism

WANG Feng-jie1,2,3, ZONG Xing-yu2, DU Jun-long2, WANG Wen-sheng2, YUAN De-pei2, CHEN Xian-bing1,2△   

  1. 1. Minda Hospital of Hubei Minzu University, Enshi 445000;
    2. Medical School of Hubei Minzu University, Enshi 445000;
    3. Science and Technology School of Hubei Minzu University, Enshi 445000, China
  • Received:2019-01-24 Online:2019-09-28 Published:2020-01-02

Abstract: Objective: To investigate the effects of dihydromyricetin (DHM) on the migration and invasion of human gastric cancer MKN45 cells and its mechanism and provide experimental basis for the prevention and treatment of gastric cancer with Traditional Chinese Medicine (TCM). Methods: MKN45 cells were pre-treated with DHM (0,10,20,30,40,50 μmol/L) for 24 and 48 hours respectively. Cell viability treated with different concentrations of DHM was detected by Cell Counting kit (CCK-8) assay, cell migration was measured by wound healing assay, and cell invasion was tested by Transwell assay. Cells were pre-treated with DHM or co-treated with c-Jun N-terminal kinase (JNK) pathway inhibitor SP600125, then, the levels of migration- and invasion-related proteins were tested by Western blot. Results: DHM concentration-dependently inhibited cell migration and invasion and downregulated matrix metalloprotein -2 (MMP-2) and phosphorylated JNK (pJNK) expression in MKN45 cells, followed by upregulation of E-cadherin and downregulation of Vimentin. Co-treatment with DHM and JNK inhibitor SP600125 further suppressed MMP-2 expression and cell invasion in MKN45 cells, suggesting that DHM inhibited MKN45 cells metastasis through JNK/MMP-2 pathway. Conclusion: DHM can inhibit cell migration and invasion in human gastric cancer MKN45 cells through downregulating MMP-2 expression via JNK signaling pathway and reverse epithelial-mesenchymal transition (EMT), implying that DHM could have the potential to serve as an anti-metastatic agent for treating gastric cancer.

Key words: gastric cancer MKN45 cells, dihydromyricetin, cell migration, cell invasion, JNK/MMP-2 pathway

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