title: Panax ginseng polysaccharide suppresses metastasis via modulating Twist expression in gastric cancer.
abstract: It was previously reported that an antitumor polysaccharide (PGPW1) was isolated from the root of Panax ginseng. To extend our study, we investigated here the anti-invasive and metastatic effects of PGPW1 on human gastric cancer cell line HGC-27 and tried to determine its possible mechanism of action. Both scratch wound-healing and Transwell assay identified that PGPW1 dose-dependently inhibited migration and invasiveness of HGC-27 cells. Furthermore, results of western blot showed that protein levels of Twist and AKR1C2 were inhibited by PGPW1, whereas an increase of NF1 was observed. Moreover, down-regulation of Twist expression by PGPW1 blocked epithelial-mesenchymal transition (EMT), characterized by a gain of epithelial cell markers, E-cadherin, and loss of the mesenchymal markers, vimentin and N-cadherin, at protein levels. Collectively, we confirmed that PGPW1 decreased migration and invasion of HGC-27 cells by regulation of Twist, AKR1C2, NF1, E-cadherin, vimentin and N-cadherin expression. In conclusion, PGPW1 may serve as a powerful chemopreventive agent against gastric cancer metastasis.
authors.affiliation: Department of Pathology, The Third Affiliated (Tumor) Hospital, Harbin Medical University, Harbin 150040, China.
authors.forename: Jian-Ping
authors.initials: JP
authors.lastname: Cai
authors.forename: Yang-Jiazi
authors.initials: YJ
authors.lastname: Wu
authors.forename: Cong
authors.initials: C
authors.lastname: Li
authors.forename: Mei-Yan
authors.initials: MY
authors.lastname: Feng
authors.forename: Qing-Tao
authors.initials: QT
authors.lastname: Shi
authors.forename: Rui
authors.initials: R
authors.lastname: Li
authors.forename: Zhen-Yu
authors.initials: ZY
authors.lastname: Wang
authors.forename: Jing-Shu
authors.initials: JS
authors.lastname: Geng
mesh_terms: D015703:Antigens, CD / Q000096:biosynthesis / Q000235:genetics; D015820:Cadherins / Q000096:biosynthesis / Q000235:genetics; D045744:Cell Line, Tumor; D015536:Down-Regulation / Q000187:drug effects / Q000235:genetics; D058750:Epithelial-Mesenchymal Transition / Q000187:drug effects / Q000235:genetics; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects* / Q000235:genetics; D006801:Humans; D006913:Hydroxysteroid Dehydrogenases / Q000096:biosynthesis / Q000235:genetics; D009362:Neoplasm Metastasis; D025542:Neurofibromin 1 / Q000096:biosynthesis / Q000235:genetics; D009687:Nuclear Proteins / Q000096:biosynthesis* / Q000235:genetics; D005894:Panax / Q000737:chemistry*; D011134:Polysaccharides / Q000737:chemistry / Q000494:pharmacology*; D013274:Stomach Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D051879:Twist-Related Protein 1 / Q000096:biosynthesis* / Q000235:genetics; D014746:Vimentin / Q000096:biosynthesis / Q000235:genetics; D045002:3-alpha-Hydroxysteroid Dehydrogenase (B-Specific)
chemical_list: D015703:Antigens, CD; D015820:Cadherins; D006913:Hydroxysteroid Dehydrogenases; D025542:Neurofibromin 1; D009687:Nuclear Proteins; D011134:Polysaccharides; D051879:Twist-Related Protein 1; D014746:Vimentin; C050361:CDH2 protein, human; C103173:TWIST1 protein, human; C435496:AKR1C2 protein, human; D045002:3-alpha-Hydroxysteroid Dehydrogenase (B-Specific)