Antimetastatic effects of licochalcone A on oral cancer via regulating metastasis-associated proteases

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• 作者：Huan Shen ; Guang Zeng ; Guo Tang ; Xingwei Cai ; Lixia Bi ; Changcheng Huang…
• 关键词：Licochalcone A ; Oral cancer ; Invasion ; Migration ; Metastasis ; MMP ; 2 ; TIMP ; 2 ; E ; cadherin ; N ; cadherin ; p ; p65
• 刊名：Tumor Biology
• 出版年：2014
• 出版时间：August 2014
• 年：2014
• 卷：35
• 期：8
• 页码：7467-7474
• 全文大小：575 KB
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• 作者单位：Huan Shen (1)
  Guang Zeng (2)
  Guo Tang (3)
  Xingwei Cai (1)
  Lixia Bi (1)
  Changcheng Huang (1)
  Yongjin Yang (1)
  
  1. Department of Stomatology, The General Hospital of the Second Artillery Corps of Chinese PLA, Beijing, 100088, People’s Republic of China
  2. Department of Plastic and Burn Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi’an, 710038, People’s Republic of China
  3. Department of Dermatology, The First Affiliated Hospital of the General Hospital of the People’s Liberation Army, Beijing, 100037, People’s Republic of China
  
• ISSN：1423-0380

文摘

Licochalcone A, a major phenolic constituent of the licorice species Glycyrrhiza inflata, has been proven to possess various biological benefits including anti-cancer activity. However, the detailed effects and molecular mechanisms of licochalcone A on the invasiveness and metastasis of oral cancer cells have not been fully understood. Thus, SCC-25 oral cancer cells were subjected to a treatment with licochalcone A at indicated concentrations (25, 50, and 100?μg/mL) for 36?h and then analyzed for the effect of licochalcone A on the cell migration and invasion. In vitro assays, including wound healing, cell adhesion, and cell invasion/migration assays, revealed that licochalcone A treatment significantly inhibited the cell migration/invasion capacities of SCC-25 cells. Also, results of zymography and Western blotting showed that activity and protein level of matrix metalloproteinase-2 (MMP-2) was suppressed, but TIMP-2 level was increased, indicating the important role of MMP-2 and TIPM-2 in anti-metastatic regulation of SCC-25 cells. Furthermore, licochalcone A was shown to suppress the nuclear factor-kappa B (NF-κB) signal, as evidenced by the decreased expression of phosphorylated p65 (p-65) protein in licochalcone A-treated SCC-25 cells. Notably, we also found that licochalcone A treatment increased the expression of the epithelial marker E-cadherin and decreased the expression of mesenchymal markers N-cadherin in SCC-25 cells. This is the first report describing the effects and possible mechanisms of licochalcone A on tumor invasion and metastasis of SCC-25 cells. Taken together, our findings support that licochalcone A can be developed to a potent anti-metastatic candidate for oral cancer therapy.