論文

査読有り 国際誌
2018年9月

Bufalin suppresses the proliferation and metastasis of renal cell carcinoma by inhibiting the PI3K/Akt/mTOR signaling pathway.

Oncology letters
  • Jinlin Xie
  • ,
  • Wenfeng Lin
  • ,
  • Linglong Huang
  • ,
  • Naijin Xu
  • ,
  • Abai Xu
  • ,
  • Binshen Chen
  • ,
  • Masami Watanabe
  • ,
  • Chunxiao Liu
  • ,
  • Peng Huang

16
3
開始ページ
3867
終了ページ
3873
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.3892/ol.2018.9111

Bufalin, one of the active ingredients of the Chinese drug Chan su, exhibits significant antitumor activity against various cancer types. However, the role of bufalin in renal cell carcinoma (RCC) remains unclear. In the present study, it was demonstrated that bufalin inhibited cell proliferation, blocked the cell cycle in the G2/M phase, and reduced the metastasis of human RCC ACHN cells via the upregulation of p21waf/cip1 and E-cadherin and the downregulation of cyclin dependent kinase 1, cyclin B1, N-cadherin, and hypoxia-inducible factor-1α (HIF-1α). Further mechanistic study revealed that bufalin reduced the expression of phosphorylated (phospho)-Akt and phospho-mammalian target of rapamycin (mTOR). Moreover, HIF-1α expression may be regulated through the inhibition of the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mTOR signaling pathway. Thus, the present results suggest that bufalin induces cell cycle arrest and suppresses metastasis; this process may be associated with the PI3K/Akt/mTOR signaling pathway. Accordingly, it is suggested that bufalin is a therapeutic agent for RCC.

リンク情報
DOI
https://doi.org/10.3892/ol.2018.9111
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/30128000
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6096133
ID情報
  • DOI : 10.3892/ol.2018.9111
  • PubMed ID : 30128000
  • PubMed Central 記事ID : PMC6096133

エクスポート
BibTeX RIS