Sorafenib suppresses the epithelial-mesenchymal transition of hepatocellular carcinoma cells after insufficient radiofrequency ablation
Autor: | Wenbing Sun, Lian Chen, Jinge Kong, Shuying Dong, Bing Pan, Jian Kong, Liang Ji, Fandong Kong, Jun Gao, Lemin Zheng |
---|---|
Rok vydání: | 2014 |
Předmět: |
Sorafenib
Niacinamide Pathology medicine.medical_specialty Cancer Research Carcinoma Hepatocellular Epithelial-Mesenchymal Transition Radiofrequency ablation Cell Survival Hepatocellular carcinoma Antineoplastic Agents law.invention Mice In vivo law Cell Movement Cell Line Tumor Carcinoma medicine Genetics Animals Humans MTT assay Neoplasm Invasiveness Epithelial–mesenchymal transition neoplasms business.industry Phenylurea Compounds Liver Neoplasms Hep G2 Cells medicine.disease Xenograft Model Antitumor Assays digestive system diseases Gene Expression Regulation Neoplastic Insufficient radiofrequency ablation surgical procedures operative Oncology Cancer research Catheter Ablation Stem cell business therapeutics medicine.drug Research Article |
Zdroj: | BMC Cancer |
ISSN: | 1471-2407 |
Popis: | Background Epithelial-mesenchymal transition (EMT) played an important role in the progression of hepatocellular carcinoma (HCC) after insufficient radiofrequency ablation (RFA). However, whether sorafenib could be used to suppress the EMT of HCC after insufficient RFA and further prevent the progression of residual HCC remains poorly unknown. Methods Insufficient RFA was simulated using a water bath (47 °C 5, 10, 15, 20 and 25 min gradually). MTT assay and transwell assay were used to evaluate the effects of sorafenib on viability, migration and invasion of HepG2 and SMMC7721 cells after insufficient RFA in vitro. After insufficient RFA, the molecular changes in HCC cells with the treatment of sorafeinb were evaluated using western blot and ELISAs. An ectopic nude mice model was used to evaluate the effect of sorafenib on the growth of HepG2 cells in vivo after insufficient RFA. Results HepG2 and SMMC7721 cells after insufficient RFA (named as HepG2-H and SMMC7721-H) exhibited enhanced viability, migration and invasion in vitro. Sorafenib inhibited the enhanced viability, migration and invasion of HepG2 and SMMC7721 cells after insufficient RFA. Molecular changes of EMT were observed in HepG2-H and SMMC7721-H cells. Sorafenib inhibited the EMT of HepG2-H and SMMC7721-H cells. HepG2-H cells also exhibited larger tumor size in vivo. Higher expression of PCNA, Ki67, N-cadherin, MMP-2 and MMP-9, was also observed in HepG2-H tumors. Sorafenib blocked the enhanced growth of HepG2 cells in vivo after insufficient RFA. Conclusions Sorafenib inhibited the EMT of HCC cells after insufficient RFA, and may be used to prevent the progression of HCC after RFA. Electronic supplementary material The online version of this article (doi:10.1186/s12885-015-1949-7) contains supplementary material, which is available to authorized users. |
Databáze: | OpenAIRE |
Externí odkaz: |