4',7-Isoflavandiol
4',7-Isoflavandiol, an estrogen metabolite, affects the ability of soy nuts to improve cardiovascular risk factors. 4',7-Isoflavandiol is a potential anticancer agent against HeLa, with possible mechanisms involved in ROS generation and mitochondrial membrane alteration; it may advance breast cancer potential via up-regulation of the eukaryotic initiation factor 4GI (eIF4GI).
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to
24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
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Anticancer Res. 2014 Sep;34(9):4985-92.
Equol induces mitochondria-mediated apoptosis of human cervical cancer cells.[Pubmed:
25202081]
The present study aimed to investigate anticancer properties of 4',7-Isoflavandiol and demonstrate its underlying mechanisms of action in human cervical cancer HeLa cells.
METHODS AND RESULTS:
Inhibition of cell viability was examined by 3-(4,5-dimethylthiazoly-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Apoptosis was evaluated by observation of apoptotic cell morphology, and an increase of annexin-V(+) cells. Western blotting was used to examine apoptosis-related proteins. Flow cytometry was used to measure mitochondrial membrane potential (MMP) and reactive oxygen species (ROS). 4',7-Isoflavandiol treatment inhibited HeLa cell proliferation in dose- and time-dependent manner. 4',7-Isoflavandiol-induced apoptotic cell death was accompanied by the activation of caspases, and alteration of MMP and mitochondrial membrane proteins; 4',7-Isoflavandiol also rapidly triggered ROS production. Pre-treatment with N-acetylcysteine blocked loss of MMP, caused increase of Bcl-2-associated X protein (Bax)/B-cell lymphoma 2 (Bcl-2) ratio, caspase-8 activation, and apoptosis induced by equol.
CONCLUSIONS:
4',7-Isoflavandiol is a potential anticancer agent against HeLa, with possible mechanisms involved in ROS generation and mitochondrial membrane alteration.
Metabolism. 2015 Feb;64(2):236-43.
Effect of soy nuts and equol status on blood pressure, lipids and inflammation in postmenopausal women stratified by metabolic syndrome status.[Pubmed:
25441251]
Soy has been associated with lower risk of cardiovascular disease in Asian countries which consume daily soy. Our study examined whether production of 4',7-Isoflavandiol , an estrogen metabolite, affected the ability of soy nuts to improve cardiovascular risk factors.
METHODS AND RESULTS:
Sixty postmenopausal women participated in a randomized, controlled, crossover trial of a Therapeutic Lifestyle Changes (TLC) diet alone and a TLC diet in which 0.5 cup of soy nuts (25 g of soy protein and 101 mg of aglycone isoflavones) replaced 25 g of nonsoy protein daily. Each diet was followed for 8 weeks at the end of which blood pressure (BP), lipid levels, adhesion molecules and inflammatory markers were measured. Women with MetS had significantly higher baseline body mass index (BMI), BP, triglycerides (TG), and soluble intercellular adhesion molecule (sICAM) than women without MetS. In women with MetS on the soy diet, significant reductions in diastolic BP (7.7%; P=0.02), TG (22.9%; P=0.02), C-reactive protein (CRP) (21.4%; P=0.01) and sICAM (7.3%; P=0.03) were noted among equol producers compared to levels on the TLC diet. No significant changes were noted in 4',7-Isoflavandiol nonproducers. Similarly, in women without MetS, only 4',7-Isoflavandiol producers had significant reductions in diastolic BP (3.3%, P=0.02) and CRP (30%, P=0.04). In contrast to women with MetS, TG and sICAM levels were not affected in women without MetS, a finding possibly related to lower baseline levels.
CONCLUSIONS:
Cardiovascular risk reduction with soy nuts is not uniform and may be greater among producers of 4',7-Isoflavandiol..
J Biol Chem. 2015 Mar 6;290(10):6047-57.
Equol, an isoflavone metabolite, regulates cancer cell viability and protein synthesis initiation via c-Myc and eIF4G.[Pubmed:
25593313]
Epidemiological studies implicate dietary soy isoflavones as breast cancer preventives, especially due to their anti-estrogenic properties. However, soy isoflavones may also have a role in promoting breast cancer, which has yet to be clarified. We previously reported that 4',7-Isoflavandiol, a metabolite of the soy isoflavone daidzein, may advance breast cancer potential via up-regulation of the eukaryotic initiation factor 4GI (eIF4GI). In estrogen receptor negative (ER-) metastatic breast cancer cells, equol induced elevated levels of eIF4G, which were associated with increased cell viability and the selective translation of mRNAs that use non-canonical means of initiation, including internal ribosome entry site (IRES), ribosome shunting, and eIF4G enhancers. These mRNAs typically code for oncogenic, survival, and cell stress molecules. Among those mRNAs translationally increased by 4',7-Isoflavandiol was the oncogene and eIF4G enhancer, c-Myc.
METHODS AND RESULTS:
Here we report that siRNA-mediated knockdown of c-Myc abrogates the increase in cancer cell viability and mammosphere formation by 4',7-Isoflavandiol , and results in a significant down-regulation of eIF4GI (the major eIF4G isoform), as well as reduces levels of some, but not all, proteins encoded by mRNAs that are translationally stimulated by 4',7-Isoflavandiol treatment. Knockdown of eIF4GI also markedly reduces an equol-mediated increase in IRES-dependent mRNA translation and the expression of specific oncogenic proteins. However, eIF4GI knockdown did not reciprocally affect c-Myc levels or cell viability.
CONCLUSIONS:
This study therefore implicates c-Myc as a potential regulator of the cancer-promoting effects of 4',7-Isoflavandiol via up-regulation of eIF4GI and selective initiation of translation on mRNAs that utilize non-canonical initiation, including certain oncogenes.
