CIIA induces the epithelial-mesenchymal transition and cell invasion

Sun Young Han, Hyun Sub Hwang, Ji Soo Chae, Suk Jin Yang, Je Hyun Yoon, Young Il Yeom, Eui Ju Choi

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)


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 down-regulation of claudin-1.

Original languageEnglish
Pages (from-to)548-552
Number of pages5
JournalBiochemical and biophysical research communications
Issue number3
Publication statusPublished - 2009 Sept 25

Bibliographical note

Funding Information:
This work was supported by the Korea Research Foundation Grant (KRF-2006-341-C00023) and by Basic Science Research Program (2009-0080895) through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science & Technology, South Korea (E.-J.C.), and by a grant from the 21C Frontier Human Genome Functional Analysis Project of the Ministry of Science and Technology of Korea (Y.I.Y.).


  • CIIA
  • Claudin-1
  • Epithelial-mesenchymal transition
  • Invasion
  • Migration

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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