PloS one, 2014-12, Vol.9 (12), p.e115949-e115949
2014
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- Autor(en) / Beteiligte
- Titel
- Incomplete radiofrequency ablation enhances invasiveness and metastasis of residual cancer of hepatocellular carcinoma cell HCCLM3 via activating β-catenin signaling
- Ist Teil von
- PloS one, 2014-12, Vol.9 (12), p.e115949-e115949
- Ort / Verlag
- United States: Public Library of Science
- Erscheinungsjahr
- 2014
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- Radiofrequency ablation (RFA) is one of the curative therapies for hepatocellular carcinoma (HCC), however, accelerated progression of residual HCC after incomplete RFA has been reported more frequently. The underlying molecular mechanism of this phenomenon remains to be elucidated. In this study, we used an incomplete RFA orthotopic HCC nude mouse model to study the invasive and metastatic potential of residual cancer as well as the correlated mechanism. The incomplete RFA orthotopic nude mouse models were established using high metastatic potential HCC cell line HCCLM3 and low metastatic potential HCC cell line HepG2, respectively. The changes in cellular morphology, motility, metastasis and epithelial-mesenchymal transition (EMT), and HCC cell molecular markers after in vitro and in vivo incomplete RFA intervention were observed. Pulmonary and intraperitoneal metastasis were observed in an in vivo study. The underlying pro-invasive mechanism of incomplete RFA appeared to be associated with promoting EMT, including down-regulation of E-cadherin and up-regulation of N-cadherin and vimentin. These results were in accordance with the in vitro response of HCC cells to heat intervention. Further studies demonstrated that β-catenin was a pivotal factor during this course and blocking β-catenin reduced metastasis and EMT phenotype changes in heat-treated HCCLM3 cells in vitro. Incomplete RFA enhanced the invasive and metastatic potential of residual cancer, accompanying with EMT-like phenotype changes by activating β-catenin signaling in HCCLM3 cells.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1932-6203eISSN: 1932-6203DOI: 10.1371/journal.pone.0115949Titel-ID: cdi_plos_journals_1640559812
- Format
- –
- Schlagworte
- Ablation, Animal models, Animals, beta Catenin - metabolism, Cadherins - metabolism, Cancer, Carcinoma, Hepatocellular - metabolism, Carcinoma, Hepatocellular - pathology, Carcinoma, Hepatocellular - surgery, Cell adhesion & migration, Cell Line, Tumor, Cell Movement, Colorectal cancer, Cytology, E-cadherin, Education, Epithelial-Mesenchymal Transition, Heat treatment, Hep G2 Cells, Hepatocellular carcinoma, Hot Temperature, Humans, Hypoxia, In vivo methods and tests, Intervention, Invasiveness, Laboratories, Liver - metabolism, Liver - pathology, Liver - surgery, Liver cancer, Liver Neoplasms - metabolism, Liver Neoplasms - pathology, Liver Neoplasms - surgery, Male, Medicine and Health Sciences, Mesenchyme, Metastases, Metastasis, Mice, Inbred BALB C, Mice, Nude, Mutation, N-Cadherin, Neoplasm Invasiveness - pathology, Neoplasm Metastasis - pathology, Neoplasm, Residual - etiology, Neoplasm, Residual - metabolism, Neoplasm, Residual - pathology, Proteins, Radio frequency, Radiofrequency ablation, Signal transduction, Signaling, Tumors, Vimentin, Wnt Signaling Pathway, β-Catenin