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Author Notes:

Correspondence: Dr Hai-An Fu, Department of Pharmacology and Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA 30322, USA; E-mail: hfu@emory.edu.

Dr Xu Zhang, The Pre-clinical Medicine College, Nanjing University of Chinese Medicine, Nanjing 210046, P.R. China; E-mail: zhangxu@njutcm.edu.cn

Acknowledgments: We thank members of the Fu laboratory, Emory University and Jiangsu key laboratory for TCM formulae research, Nanjing University of Chinese Medicine for assistance and enlightening discussions.


Research Funding:

This study was supported in part by National Science and Technology Pillar Program in the 11th Five-year Plan of China 2006BAI11B08-01 (to H.F. and X.Z), the Priority Academic Program Development (PAPD) of Jiangsu Higher Education Institutions (to X.Z), the Research and Innovation Program of Postgraduates in Jiangsu Province (to M.C.).


  • autophagy
  • natural medicines
  • non-small cell lung cancer
  • Ophiopogonin B
  • PI3K/Akt/mTOR

Ophiopogonin B-induced autophagy in non-small cell lung cancer cells via inhibition of the PI3K/Akt signaling pathway

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Journal Title:

Oncology Reports


Volume 29, Number 2


, Pages 430-436

Type of Work:

Article | Final Publisher PDF


Ophiopogonin B (OP-B) is a bioactive component of Radix Ophiopogon Japonicus, which is often used in Chinese traditional medicine to treat pulmonary disease. However, whether or not OP-B has any potential antitumor activity has not been reported. Here, we show that the non-small cell lung cancer (NSCLC) cell lines NCI-H157 and NCI-H460 treated with OP-B grow more slowly and accumulate vacuoles in their cytoplasm compared to untreated control cells. Flow cytometric analysis showed that the cells were arrested in G0/G1 phase. Nuclear morphology, Annexin-V/PI staining, and expression of cleaved caspase-3 all confirm that OP-B does not induce apoptosis. Instead, based on results from both transmission electron microscopy (TEM) and the expression of microtubule-associated protein 1 light chain 3-II (LC3-II), we determined that OP-B treatment induced autophagy in both cell lines. Next, we examined the PI3K/Akt/mTOR signaling pathway and found that OP-B inhibited phosphorylation of Akt (Ser473, Thr308) in NCI-H157 cells and also inhibited several key components of the pathway in NCI-H460 cells, such as p-Akt(Ser473, Thr308), p-p70S6K (Thr389). Additionally, insulin-mediated activation of the PI3K/Akt/mTOR pathway provides evidence that activation of this pathway may correlate with induction of autophagy in H460 cells. Therefore, OP-B is a prospective inhibitor of PI3K/Akt and may be used as an alternative compound to treat NSCLC.

Copyright information:

© 2013, Spandidos Publications

This is an Open Access work distributed under the terms of the Creative Commons Attribution-Noncommercial 3.0 Unported License (http://creativecommons.org/licenses/by-nc/3.0/).

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