1. Bufalin suppresses the proliferation and metastasis of renal cell carcinoma by inhibiting the PI3K/Akt/mTOR signaling pathway
- Author
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Abai Xu, Chunxiao Liu, Linglong Huang, Wenfeng Lin, Masami Watanabe, Binshen Chen, Jinlin Xie, Peng Huang, and Naijin Xu
- Subjects
0301 basic medicine ,renal cell carcinoma ,Cancer Research ,Cyclin-dependent kinase 1 ,Cell cycle checkpoint ,Cell growth ,Chemistry ,Bufalin ,p-Akt ,Articles ,cycle arrest ,Cell cycle ,03 medical and health sciences ,030104 developmental biology ,0302 clinical medicine ,Oncology ,030220 oncology & carcinogenesis ,Cancer research ,metastasis ,bufalin ,Cyclin B1 ,Protein kinase B ,PI3K/AKT/mTOR pathway - Abstract
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.
- Published
- 2018