Dioscin suppresses human laryngeal cancer cells growth via induction of cell-cycle arrest and MAPK-mediated mitochondrial-derived apoptosis and inhibition of tumor invasion

Si, Lingling; Zheng, Liqin; Xu, Lina; Yin, Lianhong; Han, Xu; Qi, Yan; Xu, Youwei; Wang, Changyuan; Peng, Jinyong

doi:10.1016/j.ejphar.2016.02.009

Cited by 52 publications

(31 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Dioscin (Figure S1), one such natural product, has been shown to have anti‐inflammatory, antifungal, antivirus, and antihepatic fibrosis activities (Cho, ; Liu et al, ; Lu et al, ; Wang et al, ; Zhao et al, ). In addition, dioscin shows potent effects against colon cancer, lung cancer, laryngeal cancer, and glioblastoma multiforme (Si et al, ; Wei et al, ). Moreover, dioscin can induce apoptosis and autophagy in Huh‐7 cells (Xu et al, ), suppress cell proliferation in BEL‐7402 cells (Zhang et al, ), and reverses multidrug resistance in human hepatoma HepG2/adriamycin cells (Sun et al, ).…”

Section: Introductionmentioning

confidence: 99%

Potent effects of dioscin against hepatocellular carcinoma through regulating TP53‐induced glycolysis and apoptosis regulator (TIGAR)‐mediated apoptosis, autophagy, and DNA damage

Zhang

Han

Chen

et al. 2019

British J Pharmacology

Self Cite

View full text Add to dashboard Cite

Background and purpose: Dioscin shows potent effects against cancers. We aimed to elucidate its pharmacological effects and mechanisms of action on hepatocellular carcinoma (HCC) in vivo and in vitro.Experimental approach: Effects of dioscin were investigated in SMMC7721 and HepG2 cells, diethylnitrosamine-induced primary liver cancer in rats, and cell xenografts in nude mice. Isobaric tags for relative and absolution quantitation (iTRAQ)based proteomics was used to find dioscin's targets and investigate its mechanism.Key results: In SMMC7721 and HepG2 cells dioscin markedly inhibited cell proliferation and migration, induced apoptosis, autophagy, and DNA damage. It inhibited DEN-induced primary liver cancer in rats, markedly changed body weights and restored levels of α fetoprotein, alanine transaminase, aspartate transaminase, γ-glutamyltransferase, alkaline phosphatase, and Ki67. It also inhibited growth of xenografts in mice. In SMMC7721 cells, 191 differentially expressed proteins were found after dioscin, based on iTRAQ-based assay. TP53-inducible glycolysis and apoptosis regulator (TIGAR) was identified as being significantly down-regulated by dioscin. Dioscin induced cell apoptosis, autophagy, and DNA damage via increasing expression levels of p53, cleaved PARP, Bax, cleaved caspase-3/9, Beclin-1, and LC3 and suppressing those of Bcl-2, p-Akt, p-mammalian target of rapamycin (mTOR), CDK5, p-ataxia telangiectasia-mutated gene (ATM). The transfection of TIGAR siRNA into SMMC7721 cells and xenografts in nude mice further confirmed that the potent activity of dioscin against HCC is evoked by adjusting TIGAR-mediated inhibition of p53, Akt/mTOR, and CDK5/ATM pathways. Conclusions and implications:The data suggest that dioscin has potential as a therapeutic, and TIGAR as a drug target for treating HCC.

show abstract

Section: Introductionmentioning

confidence: 99%

Potent effects of dioscin against hepatocellular carcinoma through regulating TP53‐induced glycolysis and apoptosis regulator (TIGAR)‐mediated apoptosis, autophagy, and DNA damage

Zhang

Han

Chen

et al. 2019

British J Pharmacology

Self Cite

View full text Add to dashboard Cite

show abstract

“…Dioscin is an anticancer natural product in recent years (Brahmbhatt et al, 2015;Vassilakopoulou et al, 2015;Si et al, 2016). Glucose is firstly decomposed into pyruvic acid without aerobic action, and then a tricarboxylic acid (TCA) cycle is performed in the mitochondria to produce a large amount of ATP.…”

Section: Discussionmentioning

confidence: 99%

High-Throughput Metabolomics for Identification of Metabolic Pathways and Deciphering the Effect Mechanism of Dioscin on Rectal Cancer From Cell Metabolic Profiles Coupled With Chemometrics Analysis

Wang

2020

Front. Pharmacol.

View full text Add to dashboard Cite

High-throughput liquid chromatography-mass spectrometry (LC-MS)-based metabolomics can provide the holistic analysis of the low molecular weight endogenous metabolites in cells and reflect the changes of cellular regulation and metabolic pathways. Our study designed to reveal the potentially pharmacological effects of dioscin on SW480 rectal cancer cells using nontargeted metabolomics method to probe into small molecular metabolites and pathway changes. After the cell assay of proliferation, apoptosis, migration, and invasion, the dioscin-treated cell samples were prepared for nontargeted metabolomics analysis based on LC-MS tool to describe the metabolic profiles. Dioscin has prevented cell proliferation and accelerated cell apoptosis, and it also inhibited the SW480 rectal cancer cells' migration and invasion. A total of 22 metabolites were selected as promising biomarkers of pharmacological reaction of dioscin to rectal cancer, and eight highly correlated pathways including D-glutamine and D-glutamate metabolism, pyruvate metabolism, arachidonic acid metabolism, phenylalanine metabolism, tryptophan metabolism, glycolysis or gluconeogenesis, citrate cycle (TCA cycle), and butanoate metabolism were identified. It showed that strategies based on cell metabolomics are helpful tools to discover the small molecular metabolites to elucidate the action mechanism of drug.

show abstract

“…It also has anti‐inflammatory (Wang et al, ), anti‐fungal (Cho et al, ), anti‐virus (Aquino et al, ), anti‐liver fibro s is (Zhang et al, ; Gu et al, ), anti‐obesity (Liu et al, ) and hepatoprotective activities (Lu et al, ; Zhao et al, ). In addition, dioscin shows active effects against colon cancer, lung cancer, hepatocarcinoma, esophageal cancer, laryngeal cancer and glioblastoma multiforme (Wang et al ., ,b; Wei et al, ; Chen et al, ; Si et al, ). Furthermore, dioscin can down‐regulate the level of peroxiredoxin 1 and induce ROS‐mediated apoptosis in MiaPaCa‐2 cells (Zhao et al, ), suggesting that dioscin might exert potent effects against pancreatic cancer.…”

Section: Introductionmentioning

confidence: 99%

Potent effects of dioscin against pancreatic cancer via miR‐149‐3P‐mediated inhibition of the Akt1 signalling pathway

Yin

et al. 2017

British J Pharmacology

Self Cite

View full text Add to dashboard Cite

show abstract

Dioscin suppresses human laryngeal cancer cells growth via induction of cell-cycle arrest and MAPK-mediated mitochondrial-derived apoptosis and inhibition of tumor invasion

Cited by 52 publications

References 56 publications

Potent effects of dioscin against hepatocellular carcinoma through regulating TP53‐induced glycolysis and apoptosis regulator (TIGAR)‐mediated apoptosis, autophagy, and DNA damage

Potent effects of dioscin against hepatocellular carcinoma through regulating TP53‐induced glycolysis and apoptosis regulator (TIGAR)‐mediated apoptosis, autophagy, and DNA damage

High-Throughput Metabolomics for Identification of Metabolic Pathways and Deciphering the Effect Mechanism of Dioscin on Rectal Cancer From Cell Metabolic Profiles Coupled With Chemometrics Analysis

Potent effects of dioscin against pancreatic cancer via miR‐149‐3P‐mediated inhibition of the Akt1 signalling pathway

Contact Info

Product

Resources

About