The Mechanism Of Lithospermum Erythrorhizon Extracts Shikonin-Mediated Inhibition Of Migration And Invasion In Human Non-Small Cell Lung Carcinoma

• Main Authors: Chen Wan-Shen, 陳宛伸
• Other Authors: Weng Meng-Shih
• Format: Others
• Language: zh-TW
• Published: 2015
• Online Access: http://ndltd.ncl.edu.tw/handle/bgjd9q

碩士 === 輔仁大學 === 營養科學系碩士班 === 103 === Hepatocyte growth factor (HGF)/c-MET axis is the important signaling of growth and differentiation in cancer cells. Dysregulation of HGF/c-MET signaling has been associated with tumor progression and metastasis in lung cancer. HGF/c-MET-mediated epithelial to mesenchymal transition (EMT) process has been shown to regulate lung cancer progression and metastasis. Therefore, targeting HGF/c-MET-mediated EMT process might inhibit metastasis of lung cancer. Shikonin, a naphthoquinone from the roots of lithospermum erythrorhizon, has been demonstrated to possess anti-tumor, anti-migration and invasion effects. The purpose of this study is to verify the anti-metastatic and anti-invasive effects of shikonin in lung cancer cells. Our results revealed that cell viability and cell cycle distribution did not change less than 1 μM shikonin treatment in HCC827 and A549 lung cancer cells. Interestingly, the migration and invasion activities of HCC827 and HGF-stimulated A549 lung cancer cells were inhibited by shikonin in a dose-dependent manner. Furthermore, c-MET phosphorylation and HGF/c-MET-mediated Akt and ERK phosphorylation were down-regulated by shikonin treatment in HCC827 and HGF-stimulated A549 lung cancer cells. E-cadherin, the epithelial marker of EMT, was up-regulated while vimentin, slug and snail, mesenchymal markers of EMT, were down-regulated in shikonin treated cells. Our results implicate that shikonin may inhibit migration and invasion of lung cancer cells through down-regulating HGF/c-MET-mediated EMT process.