Tumor necrosis factor-α (TNF-α) stimulates the epithelial-mesenchymal transition regulator Snail in cholangiocarcinoma

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

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

Epithelial-mesenchymal transition (EMT) is a series of events during which epithelial cells lose many of their epithelial characteristics and take on properties that are typical of mesenchymal cells that lack cell-cell adhesion properties. EMT may be activated by various types of growth factors or inflammatory cytokines. In many types of epithelial cancers, the EMT-derived tumor cells are susceptible to metastasis. During tumor progression, epithelial cells acquire a gene expression pattern closely resembling that of mesenchymal cells. This study aimed to investigate the expression of the EMT-associated transcription factor Snail and an adhesion molecule E-cadherin in cholangiocarcinoma (CCA) tissues. The effect of TNF-α on EMT activation in CCA cells was also demonstrated. The qRT-PCR analysis revealed that Snail expression significantly increased in CCA (P = 0.01) and was correlated with tumor metastasis (P = 0.02). The expression of Snail was inversely associated with E-cadherin (P = 0.004). The stimulation of TNF-α enhances migration behavior and showed significantly induced expression of Snail in CCA cell lines, whereas expression of E-cadherin and CK-19 (the epithelial marker) was reduced. Immunofluorescence analysis revealed that TNF-α-treated CCA cell lines increased nuclear translocation of Snail, whereas E-cadherin was dramatically decreased. Our findings suggest that the changes in the expression of Snail or E-cadherin might regulate EMT development in CCA resulting in promoting tumor progression. Overexpression of Snail could be used as a prognostic marker for monitoring the treatment efficiency of CCA patients.

Original languageEnglish
Pages (from-to)3083-3091
Number of pages9
JournalMedical Oncology
Volume29
Issue number5
DOIs
Publication statusPublished - 2012 Dec

Fingerprint

Epithelial-Mesenchymal Transition
Cholangiocarcinoma
Tumor Necrosis Factor-alpha
Cadherins
Neoplasms
Epithelial Cells
Neoplasm Metastasis
Cell Line
Snails
Cell Adhesion
Fluorescent Antibody Technique
Intercellular Signaling Peptides and Proteins
Cytokines
Gene Expression
Polymerase Chain Reaction

Keywords

  • Cholangiocarcinoma
  • E-cadherin
  • Epithelial-mesenchymal transition
  • Snail
  • TNF-α

ASJC Scopus subject areas

  • Oncology
  • Cancer Research
  • Hematology
  • Medicine(all)

Cite this

Techasen, A., Namwat, N., Loilome, W., Bungkanjana, P., Khuntikeo, N., Puapairoj, A., ... Yongvanit, P. (2012). Tumor necrosis factor-α (TNF-α) stimulates the epithelial-mesenchymal transition regulator Snail in cholangiocarcinoma. Medical Oncology, 29(5), 3083-3091. https://doi.org/10.1007/s12032-012-0305-x

Tumor necrosis factor-α (TNF-α) stimulates the epithelial-mesenchymal transition regulator Snail in cholangiocarcinoma. / Techasen, Anchalee; Namwat, Nisana; Loilome, Watcharin; Bungkanjana, Pornpan; Khuntikeo, Narong; Puapairoj, Anucha; Jearanaikoon, Patcharee; Saya, Hideyuki; Yongvanit, Puangrat.

In: Medical Oncology, Vol. 29, No. 5, 12.2012, p. 3083-3091.

Research output: Contribution to journalArticle

Techasen, A, Namwat, N, Loilome, W, Bungkanjana, P, Khuntikeo, N, Puapairoj, A, Jearanaikoon, P, Saya, H & Yongvanit, P 2012, 'Tumor necrosis factor-α (TNF-α) stimulates the epithelial-mesenchymal transition regulator Snail in cholangiocarcinoma', Medical Oncology, vol. 29, no. 5, pp. 3083-3091. https://doi.org/10.1007/s12032-012-0305-x
Techasen, Anchalee ; Namwat, Nisana ; Loilome, Watcharin ; Bungkanjana, Pornpan ; Khuntikeo, Narong ; Puapairoj, Anucha ; Jearanaikoon, Patcharee ; Saya, Hideyuki ; Yongvanit, Puangrat. / Tumor necrosis factor-α (TNF-α) stimulates the epithelial-mesenchymal transition regulator Snail in cholangiocarcinoma. In: Medical Oncology. 2012 ; Vol. 29, No. 5. pp. 3083-3091.
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