CIIA induces the epithelial-mesenchymal transition and cell invasion
- Authors
- Han, Sun-Young; Hwang, Hyun Sub; Chae, Ji Soo; Yang, Suk-Jin; Yoon, Je-Hyun; Yeom, Young Il; Choi, Eui-Ju
- Issue Date
- 25-Sep-2009
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- CIIA; Epithelial-mesenchymal transition; Migration; Invasion; Claudin-1
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.387, no.3, pp.548 - 552
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 387
- Number
- 3
- Start Page
- 548
- End Page
- 552
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/119300
- DOI
- 10.1016/j.bbrc.2009.07.050
- ISSN
- 0006-291X
- Abstract
- Epithelial-mesenchymal transition (EMT) and the acquisition of invasive potential are key events in tumor progression. We now show that CIIA, originally identified as an anti-apoptotic protein, induces the EMT and promotes cell migration and invasion. Ectopic expression of CIIA induced down-regulation of E-cadherin and claudin-1 as well as up-regulation of N-cadherin in MDCK cells. It also disrupted the differentiated epithelial morphology of MDCK cells grown in three-dimensional Matrigel cultures as well as increased the migration and invasion of MDCK cells in vitro. Furthermore, depletion of endogenous CIIA by RNA interference inhibited the migration and invasion of HeLa cells and this inhibition was abolished by RNA interference-mediated depletion of claudin-1. These results suggest that CIIA functions as an inducer of cell invasion, and this effect is mediated, at least in part, through clown-regulation of claudin-1 (C) 2009 Elsevier Inc. All rights reserved.
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