Phytochemical Name : Diosgenin

Properties Information
PhytoCAT-ID PhytoCAT-1583
Phytochemical name or plant extracts Diosgenin
PMID 18022396
Literature evidence These results suggested that diosgenin has the potential to advance as chemopreventive or chemotherapeutic agent for cancers that overexpress HER2.
IUPAC name (1S,2S,4S,5'R,6R,7S,8R,9S,12S,13R,16S)-5',7,9,13-tetramethylspiro[5-oxapentacyclo[10.8.0.02,9.04,8.013,18]icos-18-ene-6,2'-oxane]-16-ol
Phytochemicals’ class or type of plant extracts Steroidal saponin
Source of phytochemicals or plant Extracts Trigonella foenum-graecum Paris polyphylla
Geographical availability Trigonella foenum-graecum - Afghanistan, Iran, Iraq, Pakistan Assam, Bangladesh, China North-Central, China South-Central, East Himalaya, Myanmar, Nepal, Qinghai, Tibet, West Himalaya
Plant parts Seeds Rhizome
Other cancers Breast cancer, Leukemia, Stomach cancer, Colorectal cancer
Target gene or protein XIAP, Survivin, Bcl-2, AKT, JNK, mTOR, Cyclin D1, CDK-2, CDK-4, FAS
Gene or Protein evidence Diosgenin inhibits pAkt expression and Akt kinase activity without affecting PI3 kinase levels, resulting in the inhibition of its downstream targets, NF-kappaB, Bcl-2, survivin and XIAP. Furthermore, diosgenin inhibited the phosphorylation of Akt and mTOR, and enhanced phosphorylation of JNK. Additionally, we found that diosgenin caused G1 cell cycle arrest by downregulating cyclin D1, cdk-2 and cdk-4 expression in both ER(+) and ER(-) BCa cells resulting in the inhibition of cell proliferation and induction of apoptosis. The use of pharmacological inhibitors revealed that the modulation of Akt, mTOR and JNK phosphorylation was required for diosgenin-induced FAS suppression
Target pathways The Raf/MEK/ERK pathway, another functional downstream target of Akt, was inhibited by diosgenin in ER(+) but not in ER(-) BCa cells.
IC50 19.28±0.36 µM against MCF-7
Potency These results suggested that diosgenin has the potential to advance as chemopreventive or chemotherapeutic agent for cancers that overexpress HER2. These findings demonstrate the effect of DG on inhibiting the resilient breast CSCs which could provide a benchmark for the development of DG-based therapies in breast cancer treatment. We report here that diosgenin (DG), a naturally occurring steroidal saponin, could effectively inhibit CSCs from three breast cancer cell lines, MCF7, T47D and MDA-MB-231, by inducing apoptosis and inhibiting the CSC associated phenotypes. Thus, these results suggest that diosgenin might prove to be a potential chemotherapeutic agent for the treatment of BCa.
Cell line/ mice model MCF-7, T47D, MDA-MB-231, C6, T98G, MCF-7 and MDA-231 xenografts in nude mice
Additional information  In addition, diosgenin significantly impacted MDA-MB-231 cell migratory behavior under real-time observation. Our finding, a restoration of keratinocyte proliferation in aged skin, suggests that diosgenin may have potential as a safe health food for climacteric. In vivo, administration of diosgenin improved the epidermal thickness in the ovariectomized mice, a climacteric model, without altering the degree of fat accumulation. We also found diosgenin significantly inhibited actin polymerization, Vav2 phosphorylation and Cdc42 activation, which might be, at least in part, attributed to the anti-metastatic potential of diosgenin. In conclusion, diosgenin showed anti-tumor effects in glioblastoma cells by induction of differentiation and apoptosis and inhibition of migration, invasion, and angiogenesis. However, diosgenin did not affect Bcl-2 and Bax levels.
PubChem ID 99474
Additional PMIDs 18022396 25434486 26682367 31454535 33460752 32683533 19384950 24656238 19428439 34803015 31755890 16797625 28373842 31761382
Additional sources of information https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:523957-1 https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:539722-1
Safety Interestingly, no significant toxicity was seen in the normal breast epithelial cells (MCF-10A) following treatment with diosgenin.