1. ¹Department of Life Sciences, Division of Molecular Life Sciences and Center for Cell Signaling Research, Ewha Womans University, Seoul 120–750, Korea
2. ²Division of Radiation and Nuclear Medicine Radiation Medicine Branch, National Caner Cancer, Gyeonggi 411–764, Korea
3. ³Department of Bioscience and Biotechnology, Institute of Bioscience, Sejong University, Seoul 143–747, Korea
4. ⁴Department of Cell Biology and Cell Adhesion, Matrix Research Center, University of Alabama at Birmingham, Birmingham, AL 35294, USA

Correspondence: E-S Oh, Center for Cell Signaling Research, Ewha Womans University, Daehyun-dong, Seodaemoon-Gu, Seoul 120–750, Korea. E-mail: OhES@mm.ewha.ac.kr

Received 5 February 2002; Revised 19 August 2002; Accepted 24 September 2002.

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 -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.