title: Sorafenib suppresses the epithelial-mesenchymal transition of hepatocellular carcinoma cells after insufficient radiofrequency ablation.
abstract: 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.
authors.affiliation: Department of Hepatobiliary Surgery, Beijing Chao-yang Hospital, Capital Medical University, Beijing, 100043, China. shuying19870219@163.com.
authors.forename: Shuying
authors.initials: S
authors.lastname: Dong
authors.affiliation: Department of Hepatobiliary Surgery, Beijing Chao-yang Hospital, Capital Medical University, Beijing, 100043, China. kongjian198@163.com.
authors.forename: Jian
authors.initials: J
authors.lastname: Kong
authors.affiliation: Department of Neurobiology, School of Basic Medical Sciences, The Neuroscience Research Institute, Peking University, Beijing, 100191, China. paul95dong46@163.com.|Key Laboratory for Neuroscience, Ministry of Education/National Health and Family Planning Commission, Peking University, Beijing, 100191, China. paul95dong46@163.com.
authors.forename: Fandong
authors.initials: F
authors.lastname: Kong
authors.affiliation: Department of Neurobiology, School of Basic Medical Sciences, The Neuroscience Research Institute, Peking University, Beijing, 100191, China. jingekong8567@gmail.com.|Key Laboratory for Neuroscience, Ministry of Education/National Health and Family Planning Commission, Peking University, Beijing, 100191, China. jingekong8567@gmail.com.
authors.forename: Jinge
authors.initials: J
authors.lastname: Kong
authors.affiliation: Department of Hepatobiliary Surgery, Beijing Chao-yang Hospital, Capital Medical University, Beijing, 100043, China. gaojun8430@163.com.
authors.forename: Jun
authors.initials: J
authors.lastname: Gao
authors.affiliation: School of Basic Medical Sciences, and Key Laboratory of Molecular Cardiovascular Sciences of Ministry of Education, The Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, Peking University Health Science Center, Beijing, 100191, China. amphitritejil@gmail.com.
authors.forename: Liang
authors.initials: L
authors.lastname: Ji
authors.affiliation: School of Basic Medical Sciences, and Key Laboratory of Molecular Cardiovascular Sciences of Ministry of Education, The Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, Peking University Health Science Center, Beijing, 100191, China. panbintz@163.com.
authors.forename: Bing
authors.initials: B
authors.lastname: Pan
authors.affiliation: The 8th Department of Orthopaedics, Affiliated Mindong Hospital of Fujian Medical University, Fujian, 355000, China. yiyuan123_0@sohu.com.
authors.forename: Lian
authors.initials: L
authors.lastname: Chen
authors.affiliation: School of Basic Medical Sciences, and Key Laboratory of Molecular Cardiovascular Sciences of Ministry of Education, The Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, Peking University Health Science Center, Beijing, 100191, China. Zhengl@bjmu.edu.cn.
authors.forename: Lemin
authors.initials: L
authors.lastname: Zheng
authors.affiliation: Department of Hepatobiliary Surgery, Beijing Chao-yang Hospital, Capital Medical University, Beijing, 100043, China. cyhswb@qq.com.
authors.forename: Wenbing
authors.initials: W
authors.lastname: Sun
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000008:administration & dosage* / Q000494:pharmacology; D006528:Carcinoma, Hepatocellular / Q000188:drug therapy* / Q000378:metabolism / Q000601:surgery; D017115:Catheter Ablation; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D058750:Epithelial-Mesenchymal Transition / Q000187:drug effects*; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D056945:Hep G2 Cells; D006801:Humans; D008113:Liver Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000601:surgery; D051379:Mice; D009361:Neoplasm Invasiveness; D009536:Niacinamide / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000494:pharmacology; D010671:Phenylurea Compounds / Q000008:administration & dosage* / Q000494:pharmacology; D000077157:Sorafenib; D023041:Xenograft Model Antitumor Assays
chemical_list: D000970:Antineoplastic Agents; D010671:Phenylurea Compounds; D009536:Niacinamide; D000077157:Sorafenib