The Impact of Icariside II on Human Prostate Cancer Cell Proliferation, Mobility, and Autophagy via PI3K-AKT-mTOR Signaling Pathway

Content Provider	Directory of Open Access Journals (DOAJ)
Author	Liu Y. Li S. Xie Y. Wang Y. Zhan Y.
Abstract	Shuang Li,* Yunlu Zhan,* Yingwei Xie,* Yonghui Wang, Yuexin Liu Department of Urology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yuexin LiuDepartment of Urology, Beijing Tongren Hospital, Capital Medical University, No. 1, Dongjiaomin Lane, Dongcheng District, Beijing 100730, People’s Republic of ChinaTel +86 13701076733Fax +86 10-58268536Email doctorlyx@126.comIntroduction: The flavonol glycoside icariside II (ICA II) has been shown to exhibit a range of anti-tumor properties. Herein, we evaluated the impact of ICA II on human prostate cancer cell proliferation, motility, and autophagy, and we further evaluated the molecular mechanisms underlying these effects.Methods: We treated DU145 human prostate cancer cells with a range of ICA II doses and then assessed their proliferation via CCK-8 assay, while flow cytometry was used to monitor apoptosis and cell cycle progression. We further utilized wound healing and transwell assays to probe the impact of ICA II on migration and invasion, and assessed autophagy via laser confocal fluorescence microscopy. Western blotting was further utilized to measure LC3-II/I, Beclin-1, P70S6K, PI3K, AKT, mTOR, phospho-AKT, phospho-mTOR, and phospho-P70S6K levels, with qRT-PCR being used to evaluate the expression of specific genes at the mRNA level.Results: We found that ICA II was capable of mediating the dose- and time-dependent suppression of DU145 cell proliferation, causing these cells to enter a state of cell cycle arrest and apoptosis. We further determined that ICA II treatment was associated with significant impairment of prostate cancer cell migration and invasion, whereas autophagy was enhanced in treated cells relative to untreated controls.Conclusion: Our results indicate that ICA II treatment is capable of suppressing human prostate tumor cell proliferation and migration while enhancing autophagy via modulating the PI3K-AKT-mTOR signaling pathway. As such, ICA II may be an ideal candidate drug for the treatment of prostate cancer.Keywords: icariside II, prostate cancer, PI3K-AKT-mTOR, autophagy, apoptosis
Related Links	https://www.dovepress.com/the-impact-of-icariside-ii-on-human-prostate-cancer-cell-proliferation-peer-reviewed-article-DDDT
e-ISSN	11778881
Journal	Drug Design, Development and Therapy
Volume Number	14
Language	English
Publisher	Dove Medical Press
Publisher Date	2020-01-01
Publisher Place	United Kingdom
Access Restriction	Open
Subject Keyword	Therapeutics. Pharmacology Icariside Ii Prostate Cancer Pi3k-akt-mtor Autophagy Apoptosis
Content Type	Text
Resource Type	Article