論文

最終著者 責任著者 国際誌
2021年8月14日

PolyI:C suppresses TGF-β1-induced Akt phosphorylation and reduces the motility of A549 lung carcinoma cells.

Molecular biology reports
  • Takahiro Yamaguchi
  • ,
  • Teizo Yoshimura
  • ,
  • Toshiaki Ohara
  • ,
  • Masayoshi Fujisawa
  • ,
  • Gao Tong
  • ,
  • Akihiro Matsukawa

48
9
開始ページ
6313
終了ページ
6321
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1007/s11033-021-06625-1

BACKGROUNDS: Epithelial mesenchymal transition (EMT) is a critical process involved in the invasion and metastasis of cancer, including lung cancer (LC). Transforming growth factor (TGF)-β is one of factors capable of inducing EMT. Polyinosinic-polycytidylic acid (polyI:C), a synthetic agonist for toll-like receptor (TLR) 3, can enhance immune responses and has been used as an adjuvant for cancer vaccines; however, it remains unclear whether it influences other process, such as EMT. In the present study, we examined the effects of polyI:C on TGF-β-treated A549 human LC cells. METHODS AND RESULTS: By in vitro cell proliferation assay, polyI:C showed no effect on the growth of A549 cells treated with TGF-β1 at the concentration range up to 10 μg/ml; however, it markedly suppressed the motility in a cell scratch and a cell invasion assay. By Western blotting, polyI:C dramatically decreased TGF-β1-induced Ak strain transforming (Akt) phosphorylation and increased phosphatase and tensin homologue (PTEN) expression without affecting the Son of mothers against decapentaplegic (Smad) 3 phosphorylation or the expression level of E-cadherin, N-cadherin or Snail, indicating that polyI:C suppressed cell motility independently of the 'cadherin switching'. The Akt inhibitor perifosine inhibited TGF-β1-induced cell invasion, and the PTEN-specific inhibitor VO-OHpic appeared to reverse the inhibitory effect of polyI:C. CONCLUSION: PolyI:C has a novel function to suppress the motility of LC cells undergoing EMT by targeting the phosphatidylinositol 3-kinase/Akt pathway partly via PTEN and may prevent or reduce the metastasis of LC cells.

リンク情報
DOI
https://doi.org/10.1007/s11033-021-06625-1
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/34390443
ID情報
  • DOI : 10.1007/s11033-021-06625-1
  • PubMed ID : 34390443

エクスポート
BibTeX RIS