Objective To investigate the role of tumor necrosis factor-α (TNF-α) in epithelial-mesenchymal transition (EMT) of hepatocellular carcinoma (HCC) cells and the related mechanism. Methods HCC cell lines Hep3B and SMMC-7721 were treated with TNF-α for 24 h; then the cell morphological changes were observed by microscope and the expressions of the epithelial markers (E- cadherin and β-catenin), mesenchymal markers (Vimentin and N-cadherin), and EMT associated transcriptional factor Twist were examined by RT-PCR and Western blotting analysis. The invasion and metastasis ability was evaluated by Transwell and wound healing assay. Luciferase reporter assay and immunofluorescence were used to determine NF-κB transcriptional activity; Western blotting analysis was used to examine the expression levels of IκBα and p-IκBα protien. Cells was also incubated with TNF-α and NF-κB inhibitor (BAY11-7082) together, and then the phenotypeof EMT was detected by microscope, RT-PCR and Western blotting analysis. Results Hep3B and SMMC-7721 cells had EMT phenotype after treated with TNF-α. Wound healing assay showed that the wound healing rate of cells exposed to TNF-α was significantly increased compared with the non-treated group (P<0. 05), and Transwell assay showed that more cells penetrating the membrane after treatment with TNF-α (P < 0. 05). TNF-α effectively promoted IκBα phosphorylation and the subsequent NF-κB nuclear translocation We also found that TNF-α-mediated EMT could be converted by NF-κB inhibitor (BAY11-7082) (P<0. 05). Conclusion TNF-α induces EMT of HCC cells through NF-κB-dependent pathways, and subsequently promotes the invasion and metastasis of HCC.

Background:Microwave therapy is a minimal invasive procedure and has been employed in clinical practice for the treatment of various types of cancers.However,its therapeutic application in non-small-cell lung cancer and the underlying mechanism remains to be investigated.This study aimed to investigate its effect on Lewis lung carcinoma (LLC) tumor in vivo.Methods:Fifty LLC tumor-bearing C57BL/6 mice were adopted to assess the effect of microwave radiation on the growth and apoptosis of LLC tumor in vivo.These mice were randomly assigned to 10 groups with 5 mice in each group.Five groups were treated by single pulse microwave at different doses for different time,and the other five groups were radiated by multiple-pulse treatment of a single dose.Apoptosis of cancer cells was determined by terminal deoxynucleotidyl transferase dUTP nick-end labeling assay.Western blotting was applied to detect the expression of proteins.Results:Single pulse of microwave radiation for 5 min had little effect on the mice.Only 15-min microwave radiation at 30 mW/cm2 significantly increased the mice body temperature (2.20 ± 0.82)℃ as compared with the other groups (0.78 ± 0.29 ℃,1.24 ± 0.52 ℃,0.78 ± 0.42 ℃,respectively),but it did not affect the apoptosis of LLC tumor cells significantly.Continous microwave radiation exposure,single dose microwave radiation once per day for up to seven days,inhibited cell division and induced apoptosis of LLC tumor cells in a dose-and duration-dependent manner.It upregulated the protein levels of p53,Caspase 3,Bax and downregulated Bcl-2 protein.Conclusions:Multiple exposures of LLC-bearing mice to microwave radiation effectively induced tumor cell apoptosis at least partly by upregulating proapoptotic proteins and downregulating antiapoptotic proteins.Continuous radiation at low microwave intensity for a short time per day is promising in treating non-small-cell lung cancer.