Loss of E-cadherin promotes migration and invasion of cholangiocarcinoma cells and serves as a potential marker of metastasis

Anchalee Techasen, Watcharin Loilome, Nisana Namwat, Narong Khuntikeo, Anucha Puapairoj, Patcharee Jearanaikoon, Hideyuki Saya, Puangrat Yongvanit

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Tumor progression is characterized by loss of cell adhesion and increase of invasion and metastasis. E-cadherin, a cell adhesion molecule, is frequently downregulated and has been proposed as an important mediator in epithelial-mesenchymal transition (EMT) in tumors. In this study, we investigated the expression of E-cadherin and its association with cancer invasion and prognosis in cholangiocarcinoma (CCA). Immunohistochemistry results demonstrated a statistically significant association between the positive metastasis status with low E-cadherin protein expression in human CCA tissues (P = 0.04). Statistical trends were identified for low E-cadherin level and shorter survival time (P = 0.08). Targeting the E-cadherin expression in CCA cells with siRNA caused upregulation of vimentin, a mesenchymal marker, and disappearance of the E-cadherin/β-catenin adhesion complex from cell membranes. Moreover, migration and invasion abilities of the cells were increased under this condition. These findings suggest that reduction of E-cadherin contributes to CCA progression by attenuating the strength of cellular adhesion, which affects motility as well as regulating the expression of EMT-related genes during CCA invasion and metastasis. Thus, E-cadherin can act as a central modulator of tumor cell phenotype and is a potential metastasis marker in CCA.

Original languageEnglish
Pages (from-to)8645-8652
Number of pages8
JournalTumor Biology
Volume35
Issue number9
DOIs
Publication statusPublished - 2014 Oct 9

Fingerprint

Cholangiocarcinoma
Cadherins
Neoplasm Metastasis
Epithelial-Mesenchymal Transition
Neoplasms
Catenins
Cell Adhesion Molecules
Vimentin
Cell Adhesion
Small Interfering RNA
Up-Regulation
Down-Regulation
Immunohistochemistry
Cell Membrane
Phenotype
Survival

Keywords

  • Cholangiocarcinoma
  • E-cadherin
  • Metastasis
  • Metastasis marker

ASJC Scopus subject areas

  • Cancer Research
  • Medicine(all)

Cite this

Techasen, A., Loilome, W., Namwat, N., Khuntikeo, N., Puapairoj, A., Jearanaikoon, P., ... Yongvanit, P. (2014). Loss of E-cadherin promotes migration and invasion of cholangiocarcinoma cells and serves as a potential marker of metastasis. Tumor Biology, 35(9), 8645-8652. https://doi.org/10.1007/s13277-014-2087-6

Loss of E-cadherin promotes migration and invasion of cholangiocarcinoma cells and serves as a potential marker of metastasis. / Techasen, Anchalee; Loilome, Watcharin; Namwat, Nisana; Khuntikeo, Narong; Puapairoj, Anucha; Jearanaikoon, Patcharee; Saya, Hideyuki; Yongvanit, Puangrat.

In: Tumor Biology, Vol. 35, No. 9, 09.10.2014, p. 8645-8652.

Research output: Contribution to journalArticle

Techasen, A, Loilome, W, Namwat, N, Khuntikeo, N, Puapairoj, A, Jearanaikoon, P, Saya, H & Yongvanit, P 2014, 'Loss of E-cadherin promotes migration and invasion of cholangiocarcinoma cells and serves as a potential marker of metastasis', Tumor Biology, vol. 35, no. 9, pp. 8645-8652. https://doi.org/10.1007/s13277-014-2087-6
Techasen, Anchalee ; Loilome, Watcharin ; Namwat, Nisana ; Khuntikeo, Narong ; Puapairoj, Anucha ; Jearanaikoon, Patcharee ; Saya, Hideyuki ; Yongvanit, Puangrat. / Loss of E-cadherin promotes migration and invasion of cholangiocarcinoma cells and serves as a potential marker of metastasis. In: Tumor Biology. 2014 ; Vol. 35, No. 9. pp. 8645-8652.
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