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Duchesnea indica extract suppresses the migration of human lung adenocarcinoma cells by inhibiting epithelial–mesenchymal transition
Author(s) -
Chen PeiNi,
Yang ShunFa,
Yu ChengChia,
Lin ChinYin,
Huang ShihHan,
Chu ShuChen,
Hsieh YihShou
Publication year - 2017
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.22420
Subject(s) - epithelial–mesenchymal transition , vimentin , fibronectin , mesenchymal stem cell , chemistry , cell , cell adhesion , plasminogen activator , cell migration , cancer research , microbiology and biotechnology , a549 cell , vitronectin , biology , immunology , biochemistry , downregulation and upregulation , immunohistochemistry , endocrinology , gene
Epithelial–mesenchymal transition (EMT) is a process through which epithelial cells are transformed into mesenchymal cells; EMT diminishes cell polarity and cell–cell adhesion in cancer cells, leading to enhanced migratory and invasive properties. In this experiment, zymography, cell invasion, and migration assays were performed. Results indicated that Duchesnea indica extracts (DIE) inhibited highly metastatic A549 and H1299 cells by reducing the secretions of matrix metalloproteinase‐2 and urokinase‐type plasminogen activator. Cell adhesion assay also demonstrated that DIE reduced the cell adhesion properties. Western blot analysis showed that DIE down‐regulated the expression of N‐cadherin, fibronectin, and vimentin, which are mesenchymal markers, and enhanced that of E‐cadherin, which is an epithelial marker. In vivo study showed that tumor growth was significantly reduced in BALB/c nude mouse xenograft model administered with oral gavage of DIE. Therefore, DIE could be exhibits potential as a phytochemical‐based platform for prevention and treatment of lung cancer. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 2053–2063, 2017.