Diosgenin inhibits osteoclastogenesis, invasion, and proliferation through the downregulation of Akt, IκB kinase activation and NF-κB-regulated gene expression

Shishodia, Shishir; Aggarwal, Bharat B.

doi:10.1038/sj.onc.1209194

Cited by 170 publications

(126 citation statements)

References 43 publications

(58 reference statements)

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“…Recently this group has made great progress to fully characterize the NF-B-mediated signaling pathway by isolating and testing the inhibitory activity of several plant-derived natural compounds (1). Among these, curcumin (2,3), and many other polyphenol derivatives (31,32,33,46,49,52,53,54) have been found to inhibit NF-B pathway in several tumor cell lines and at different levels, from I B phosphorylation to the expression of NF-B-regulated gene products. These novel findings could be of great importance in cancer prevention and therapy (27), especially in light of the latest evidence that demonstrates a pivotal role for NAD(P)H:quinone oxidoreductase 1 (NQO1) in producing ROS downstream of TNF engagement, in keratinocytes from NQO1 -/-mice (4).…”

Section: Redox-regulated Response To Cell Surface Receptors Engagementmentioning

confidence: 99%

Redox Control of Apoptosis: An Update

Filomeni

Ciriolo

2006

Antioxidants & Redox Signaling

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The redox environment of the cell is currently thought to be extremely important to control cell growth, differentiation, and apoptosis as many redox-sensitive proteins characterize these networks. A recent, widely accepted theory is that free radicals are not only dangerous species but, at low concentration, they have been designed by evolution to participate in the maintenance of cellular redox (reduction/oxidation) homeostasis. This notion derives from the evidence that cells constantly generate free radicals both as waste products of aerobic metabolism and in response to a large variety of stimuli. Free radicals, once produced, provoked cellular responses (redox regulation) against oxidative stress transducing the signals to maintain the cellular redox balance. Growing evidence suggests that in many instances the production of radical species is tightly regulated and their downstream targets are very specific, indicating that reactive oxygen species and reactive nitrogen species actively participate in several cell-signalling pathways as physiological "second messengers." In this review, we provide a general overview and novel insights into the redox-dependent pathways involved in programmed cell death.

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Section: Redox-regulated Response To Cell Surface Receptors Engagementmentioning

confidence: 99%

Redox Control of Apoptosis: An Update

Filomeni

Ciriolo

2006

Antioxidants & Redox Signaling

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“…yunnanensis against lung adenocarcinoma cell line were showed that this compounds have anticancer activity and their effect was dependent on structure of compounds in a certain grade (Yan et al, 2009). Also, another study by Shishodia and Aggarwal (2006) showed that diosgenin could inhibits cmyc gene expression that cmyc acts as a upregulator for hTERT gene expression. Therefore, based on these studies were showed this fact that diosgenin have anticancer activity and exert this property by several mechanisms probably with downregulation of cmyc gene expression.…”

Section: Discussionmentioning

confidence: 98%

Diosgenin Inhibits hTERT Gene Expression in the A549 Lung Cancer Cell Line

Mohammad

Ghareghomi²,

Haddadchi³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Background: Diosgenin, a steroidal saponin from a therapeutic herb, fenugreek (Trigonellafoenum-graceum L.), has been recognized to have anticancer properties. Telomerase activity is not detected in typical healthy cells, while in cancer cell telomerase expression is reactivated, therefore providing a promising cancer therapeutic target. Materials and Methods: We studied the inhibitory effect of diosgenin on human telomerase reverse transcriptase gene (hTERT) expression which is critical for telomerase activity. MTT-assays and qRT-PCR analysis were conducted to assess cytotoxicity and hTERT gene expression inhibition effects, respectively. Results: MTT results showed that IC 50 values for 24, 48 and 72h after treatment were 47, 44 and 43µM, respectively. Culturing cells with diosgenin treatment caused down-regulation of hTERT expression. Discussion: These results show that diosgenin inhibits telomerase activity by down-regulation of hTERT gene expression in the A549 lung cancer cell line

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“…Finally, diosgenin was found to exert a suppressed action on the NF-kB gene, which has been identified in the regulatory of regions of the entire antioxidative enzyme gene (Shishodia et al, 2006). In short, this present study investigated, for the first time, the potential antitoxic activities of diosgenin focusing on the reduced LPO effect and increased anti-oxidant activities.…”

Section: Discussionmentioning

confidence: 99%

Do diosgenin ameliorate urinary bladder toxic effect of cyclophosphamide and buthionine sulfoximine in experimental animal models?

Hamrita¹,

Rouissi²,

Kouidhi³

et al. 2012

Afr. J. Biotechnol.

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Urotoxicity is a troublesome complication associated with cylophosphamide (CP) and L-buthionine-SRsulfoximine (BSO) treatment in chemotherapy. With this concern in mind, this present study investigated the potential effects of diosgenin for the first time on urotoxicity induced by acute CP and BSO doses using a Swiss albino mouse model. Toxicity modulation was evaluated through measuring lipid peroxidation (LPO) and anti-oxidants in urinary bladder. The findings reveal that the diosgenin exerted a protective effect not only on LPO but also on enzymatic anti-oxidants. When compared to the controls, the CP-treated animals underwent significant decrease in the glutathione S-transferase (GST), glutathione reductase (GR), glutathione peroxidase (GP) and catalase (CAT) activities. The level of reduced glutathione (GSH) was also decreased with an increase in LPO in the CP-treated animals. BSO treatment exerted an additive toxic effect in the CP-treated animals. Interestingly, pre-treatment with the diosgenin restored the activities of all enzymes back to normal levels and to exhibit an overall protective effect on the CP and BSO induced toxicities in urinary bladder. The restoration of GSH through the treatment with the diosgenin can play an important role in reversing CP-induced apoptosis and free radical mediated LPO.

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Diosgenin inhibits osteoclastogenesis, invasion, and proliferation through the downregulation of Akt, IκB kinase activation and NF-κB-regulated gene expression

Cited by 170 publications

References 43 publications

Redox Control of Apoptosis: An Update

Redox Control of Apoptosis: An Update

Diosgenin Inhibits hTERT Gene Expression in the A549 Lung Cancer Cell Line

Do diosgenin ameliorate urinary bladder toxic effect of cyclophosphamide and buthionine sulfoximine in experimental animal models?

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