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Dioscin Induces Gallbladder Cancer Apoptosis by Inhibiting ROS-Mediated PI3K/AKT Signalling
Journal article   Open access   Peer reviewed

Dioscin Induces Gallbladder Cancer Apoptosis by Inhibiting ROS-Mediated PI3K/AKT Signalling

Xiaoling Song, Zheng Wang, Haibin Liang, Wenjie Zhang, Yuanyuan Ye, HuaiFeng Li, Yunping Hu, Yijian Zhang, Hao Weng, Jianhua Lu, …
International journal of biological sciences, v 13(6), pp 782-793
2017
DOI: https://doi.org/10.7150/ijbs.18732
PMID: 28656003
Featured in Collection :   UN Sustainable Development Goals @ Drexel
url
https://www.ijbs.com/v13p0782.pdfView
Published, Version of Record (VoR) Open
url
https://doi.org/10.7150/ijbs.18732View
Published, Version of Record (VoR) Open

Abstract

Animals Apoptosis - drug effects Apoptosis - genetics Cell Line, Tumor Cell Proliferation - drug effects Cell Proliferation - genetics Diosgenin - analogs & derivatives Diosgenin - therapeutic use Gallbladder Neoplasms - drug therapy Gallbladder Neoplasms - metabolism Glutathione - metabolism Humans Male Membrane Potential, Mitochondrial - drug effects Membrane Potential, Mitochondrial - genetics Mice Phosphatidylinositol 3-Kinases - genetics Phosphatidylinositol 3-Kinases - metabolism Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism Reactive Oxygen Species - metabolism Signal Transduction - drug effects Signal Transduction - genetics Xenograft Model Antitumor Assays
Gallbladder cancer (GBC), highly aggressive form of cancer with an extremely poor prognosis, is the most common malignancy of the biliary tract. In this study, we investigated the effects of dioscin (DSN) on human GBC and the potential mechanisms underlying these effects. The results showed that DSN significantly inhibited GBC cell proliferation and migration. Moreover, DSN induced GBC cell apoptosis via mitochondrial dependent apoptotic signalling. Reactive oxygen species (ROS) and glutathione (GSH) levels were measured, and ROS scavengers completely inhibited DSN-induced apoptosis and migration, indicating that ROS play an essential role in GBC progression. Western blot analysis showed that AKT activity was significantly downregulated after DSN treatment, and that inhibition/ectopic expression of AKT enhanced/abolished DSN-induced apoptosis but not migration. Furthermore, we confirmed the relationship between ROS and the PI3K/AKT pathway and found that DSN induced apoptosis by regulating ROS-mediated PI3K/AKT signaling. Taken together, these findings indicate that DSN induces GBC apoptosis through inhibiting ROS-mediated PI3K/AKT signalling.

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77 citations in Web of Science
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UN Sustainable Development Goals (SDGs)

This publication has contributed to the advancement of the following goals:

#3 Good Health and Well-Being

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Web of Science research areas
Biochemistry & Molecular Biology
Biology
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