https://scholars.lib.ntu.edu.tw/handle/123456789/414005
標題: | Diallyl trisulfide inhibits cell migration and invasion of human melanoma a375 cells via inhibiting integrin/facal adhesion kinase pathway | 作者: | Wang, Hsiao Chi Chu, Yung Lin SHU-CHEN HSIEH LEE-YAN SHEEN |
關鍵字: | DATS | invasion | metastasis | migration | skin cancer cells;DATS; invasion; metastasis; migration; skin cancer cells | 公開日期: | 1-十一月-2017 | 出版社: | WILEY | 卷: | 32 | 期: | 11 | 起(迄)頁: | 2352 | 來源出版物: | Environmental Toxicology | 摘要: | © 2017 Wiley Periodicals, Inc. Melanoma is the leading cause of death from skin disease due to its propensity for metastasis. Studies have shown that integrin-mediated focal adhesion kinase (FAK) signal pathway is implicated in cell proliferation, survival and metastasis of tumor cells. Our previous results indicated that diallyl trisulfide (DATS) provided its antimelanoma activity via inducing cell cycle arrest and apoptosis. The aim of this study was to explore DATS mediated antimetastatic effect and the corresponding mechanism in human melanoma A375 cells. We found that DATS exhibited an inhibitory effect on the abilities of migration and invasion in A375 cells under noncytotoxic concentrations analyzed by wound healing assays and Matrigel invasion chamber system. DATS attenuated invasion of A375 cells with characteristic of decreased activities and protein expressions of matrix metalloproteinase-2 (MMP-2) and MMP-9. Moreover, DATS exerted an inhibitory effect on cell adhesion of A375 cells, which is in correlation with the change in integrin signaling pathway. Results of Western blotting showed that DATS decreased the levels of several integrin subunits, including α4, α5, αv, β1, β3 and β4. Subsequently, DATS induced a strong decrease in total FAK, phosphorylated FAK Tyr-397,-576, −577, and disorganized F-actin stress fibers, resulting in a nonmigratory phenotype. These results suggest that the antimetastatic potential of DATS for human melanoma cells might be due to the disruption of integrin/FAK signaling pathway. |
URI: | https://scholars.lib.ntu.edu.tw/handle/123456789/414005 | ISSN: | 15204081 | DOI: | https://api.elsevier.com/content/abstract/scopus_id/85026329025 10.1002/tox.22445 |
SDG/關鍵字: | Cell adhesion; Cell death; Cell proliferation; Cells; Cytology; Dermatology; Enzymes; Oncology; Pathology; Proteins; DATS; Invasion; Metastasis; Migration; Skin cancers; Cell signaling; alpha4 integrin; alpha5 integrin; beta1 integrin; beta3 integrin; beta4 integrin; CD51 antigen; diallyl trisulfide; F actin; focal adhesion kinase; gelatinase A; gelatinase B; integrin; allyl compound; antineoplastic agent; diallyl trisulfide; focal adhesion kinase; gelatinase A; gelatinase B; integrin; sulfide; apoptosis; bioassay; cause of death; cells and cell components; concentration (composition); correlation; enzyme; enzyme activity; phenotype; protein; survival; tumor; A-375 cell line; Article; cell adhesion; cell invasion; cell viability; controlled study; drug mechanism; human; human cell; melanoma cell; metastasis inhibition; migration inhibition; priority journal; protein expression; protein phosphorylation; signal transduction; stress fiber; Western blotting; wound healing assay; cell motion; cell proliferation; drug effects; melanoma; metabolism; phosphorylation; signal transduction; skin tumor; tumor cell line; ultrastructure; Allyl Compounds; Antineoplastic Agents; Cell Adhesion; Cell Line, Tumor; Cell Movement; Cell Proliferation; Focal Adhesion Protein-Tyrosine Kinases; Humans; Integrins; Matrix Metalloproteinase 2; Matrix Metalloproteinase 9; Melanoma; Phosphorylation; Signal Transduction; Skin Neoplasms; Stress Fibers; Sulfides |
顯示於: | 食品科技研究所 |
在 IR 系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。