Journal
BIOMEDICINE & PHARMACOTHERAPY
Volume 85, Issue -, Pages 620-626Publisher
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2016.11.072
Keywords
Ginsenoside; Autophagy; Ovarian cancer
Funding
- National Natural Science Foundation of China [30973429]
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Background: Autophagy maintains cellular homeostasis through engulfing cytoplasmic proteins and organelles, and plays an important role in cancer initiation and progression. Ginsenoside 20(S)-Rg3, an active ingredient of Panax ginseng, exerts anti-cancer functions in various cancers. However, its molecular mechanisms, including its effect on autophagy, are not fully elucidated in tumor models. Methods: Ovarian cancer cell line SKOV3 was treated by various concentrations of 20(S)-Rg3. Markers of autophagy were detected by real-time PCR, western blot, immunofluorescence and immunohistochemistry. Cell viability was observed by CCK8 assays and cell migration and invasion were examined with Transwell. Results: 20(S)-Rg3 induced autophagy in SKOV3 ovarian cancer cells in a dose-dependent manner as indicated by the upregulation of autophagy-associated molecules including LC3 II, ATG5 and ATG7. The autophagy inhibitor chloroquine antagonized the inhibition of 20(S)-Rg3 on migration and invasion of SKOV3 cells, but slightly enhanced the impairment of 20(S)-Rg3 on cell viability. Immunohistochemistry staining of LC3, ATG5 and ATG7 on subcutaneous xenograft tissue sections from previously established nude mice models showed that 20(S)-Rg3 upregulated LC3, ATG5 and ATG7 as observed in cell models. Conclusion: Autophagy induction was one mechanism mediating inhibition of 20(S)-Rg3 on ovarian cancer invasive progression. (C) 2016 Elsevier Masson SAS. All rights reserved.
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