title: Decreased syndecan-2 expression correlates with trichostatin-A induced-morphological changes and reduced tumorigenic activity in colon carcinoma cells.
abstract: The inhibition of histone deacetylase activity is known to induce morphological changes of transformed cells. In this study, we investigated the effect of the specific HDAC inhibitor, trichostatin A (TSA), on colon carcinoma cell lines. Treatment of human colorectal carcinoma cells, KM1214 and KM12SM, with TSA induced distinct morphological changes. Both cell lines, which normally piled up in layers without clear boundary, became more flattened, and formed monolayers with evident boundaries between cells, with concomitant increased actin filament organization. Cell-cell interaction was not affected much, based on expression level, membrane localization, and interaction of E-cadherin with beta-catenin. In contrast, syndecan-2 expression was dramatically reduced and it was correlated with the morphological changes of colon carcinoma cells. Consistently, downregulation of syndecan-2 expression by antisense cDNA clearly mimicked the morphological changes in KM12SM and reduced anchorage-independent growth of colon cancer cells. All these results indicate that reduced syndecan-2 expression correlates with TSA-induced morphological changes and reduced tumorigenic activity in colon carcinoma cells.
authors.affiliation: Department of Life Sciences, Division of Molecular Life Sciences and Center for Cell Signalling Research, Ewha Womans University, Seoul, Korea.
authors.forename: Yeonhee
authors.initials: Y
authors.lastname: Kim
authors.forename: Haein
authors.initials: H
authors.lastname: Park
authors.forename: Yangmi
authors.initials: Y
authors.lastname: Lim
authors.forename: Innoc
authors.initials: I
authors.lastname: Han
authors.forename: Ho Jeong
authors.initials: HJ
authors.lastname: Kwon
authors.forename: Anne
authors.initials: A
authors.lastname: Woods
authors.forename: Eok-Soo
authors.initials: ES
authors.lastname: Oh
mesh_terms: D015820:Cadherins / Q000378:metabolism; D002448:Cell Adhesion / Q000187:drug effects; D002450:Cell Communication / Q000187:drug effects; D003110:Colonic Neoplasms / Q000378:metabolism* / Q000473:pathology*; D003598:Cytoskeletal Proteins / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D056572:Histone Deacetylase Inhibitors; D006801:Humans; D006877:Hydroxamic Acids / Q000494:pharmacology*; D008562:Membrane Glycoproteins / Q000096:biosynthesis* / Q000235:genetics; D009362:Neoplasm Metastasis; D011509:Proteoglycans / Q000096:biosynthesis* / Q000235:genetics; D053669:Syndecan-2; D015534:Trans-Activators / Q000378:metabolism; D014407:Tumor Cells, Cultured; D051176:beta Catenin
chemical_list: C495270:CTNNB1 protein, human; D015820:Cadherins; D003598:Cytoskeletal Proteins; D004791:Enzyme Inhibitors; D056572:Histone Deacetylase Inhibitors; D006877:Hydroxamic Acids; D008562:Membrane Glycoproteins; D011509:Proteoglycans; C508245:SDC2 protein, human; D015534:Trans-Activators; D051176:beta Catenin; D053669:Syndecan-2; C012589:trichostatin A