期刊
BRITISH JOURNAL OF CANCER
卷 105, 期 12, 页码 1885-1893出版社
SPRINGERNATURE
DOI: 10.1038/bjc.2011.452
关键词
cadherin switch; TGF-beta; epithelial-to-mesenchymal transition; cholangiocarcinoma; cancer progression
类别
资金
- Grants-in-Aid for Scientific Research [23592017] Funding Source: KAKEN
BACKGROUND: Epithelial-to-mesenchymal transition (EMT) is a fundamental process governing not only morphogenesis in multicellular organisms, but also cancer progression. During EMT, epithelial cadherin (E-cadherin) is downregulated while neural cadherin (N-cadherin) is upregulated, referred to as 'cadherin switch'. This study aimed to investigate whether cadherin switch promotes cancer progression in cholangiocarcinoma (CC). METHODS: CC cell lines were examined for migration, invasion, and morphological changes with typical EMT-induced model using recombinant TGF-beta 1. The changes in E-cadherin and N-cadherin expression were investigated during EMT. We also examined E-cadherin and N-cadherin expression in resected specimens from extrahepatic CC patients (n = 38), and the associations with clinicopathological factors and survival rates. RESULTS: TGF-beta 1 treatment activated cell migration, invasion, and fibroblastic morphological changes, especially in extrahepatic CC HuCCT-1 cells. These changes occurred with E-cadherin downregulation and N-cadherin upregulation, that is, cadherin switch. Patients with low E-cadherin expression had a significantly lower survival rate than patients with high E-cadherin expression (P = 0.0059). Patients with decreasing E-cadherin and increasing N-cadherin expression had a significantly lower survival rate than patients with increasing E-cadherin and decreasing N-cadherin expression (P = 0.017). CONCLUSION: Cadherin switch promotes cancer progression via TGF-beta-induced EMT in extrahepatic CC, suggesting a target for elucidating the mechanisms of invasion and metastasis in extrahepatic CC. British Journal of Cancer (2011) 105, 1885-1893. doi: 10.1038/bjc.2011.452 www.bjcancer.com Published online 8 November 2011 (C) 2011 Cancer Research UK
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