Hyperthermia inhibits transforming growth factor beta-induced epithelial-mesenchymal transition (EMT) in HepG2 hepatocellular carcinoma cells

Hepatogastroenterology. 2012 Oct;59(119):2059-63. doi: 10.5754/hge12404.

Abstract

Background/aims: EMT plays an essential role in tumor progression and metastasis. Hyperthermia is a potent approach for cancers with low side effects. However, the effect of hyperthermia on EMT of cancer cells is unknown.

Methodology: Cells were treated with TGF-β1 and epidermal growth factor for 96 h and then exposed to hyperthermia at 43°C for 0.5 h. Cell morphology was observed. Expressions of E-cadherin and vimentin were determined by Western blot. The protein and mRNA expressions of Snail were detected with Western blot and RT-PCR. Cell migratory capacity was evaluated.

Results: TGF-β1 induced EMT in HepG2 cells, which was evidenced by morphological, molecular and functional changes, including the formation of spindle shape and the loss of cell contact. The expression of E-cadherin was decreased but the expression of vimentin increased; also, the migratory capability was increased by 2.1±0.19-fold as compared with untreated cells. However, those effects were inhibited by the treatment of hyperthermia. Furthermore, the protein and mRNA expressions of Snail induced by TGF-β1 were also significantly inhibited by hyperthermia treatment

Conclusions: Hyperthermia can inhibit TGF-β1-induced EMT in HepG2 cells, suggesting that hyperthermia may alter the properties of metastatic potential in cancer cells and inhibit tumor metastasis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigens, CD
  • Blotting, Western
  • Cadherins / metabolism
  • Carcinoma, Hepatocellular / genetics
  • Carcinoma, Hepatocellular / metabolism*
  • Carcinoma, Hepatocellular / pathology
  • Cell Movement
  • Cell Shape
  • Epidermal Growth Factor / metabolism
  • Epithelial-Mesenchymal Transition*
  • Gene Expression Regulation, Neoplastic
  • Hep G2 Cells
  • Humans
  • Hyperthermia, Induced*
  • Liver Neoplasms / genetics
  • Liver Neoplasms / metabolism*
  • Liver Neoplasms / pathology
  • Neoplasm Invasiveness
  • RNA, Messenger / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Snail Family Transcription Factors
  • Time Factors
  • Transcription Factors / genetics
  • Transcription Factors / metabolism
  • Transforming Growth Factor beta1 / metabolism*
  • Vimentin / metabolism

Substances

  • Antigens, CD
  • CDH1 protein, human
  • Cadherins
  • RNA, Messenger
  • Snail Family Transcription Factors
  • Transcription Factors
  • Transforming Growth Factor beta1
  • Vimentin
  • Epidermal Growth Factor