Studies in cell culture and mouse models suggest possible benefits of pomegranate juice against breast cancer risk. These studies demonstrate that various constituents of pomegranates can inhibit aromatase and 17-B-hydroxysteroid dehydrogenase enzymes or have anti-estrogenic activity. Polyphenolic fractions from pomegranate fruit were assessed in vitro for their possible chemopreventive activity or as adjuvant in a therapeutic setting against human breast cancer cells.
Polyphenols obtained from fermented juice at concentrations ranging from 100 to 1,000 micro g/mL inhibited aromatase and 17-B-hydroxysteroid dehydrogenase type 1 activity by 60–80%. Human breast cancer cell lines MCF-7 and MB-MDA-231 cells were treated with fermented and fresh pomegranate juice. Polyphenols from fermented juice showed about twice the anti-proliferative effect as compared to polyphenols from fresh pomegranate juice.
Pomegranate seed oil resulted in 90% inhibition of proliferation of MCF-7 cells. Invasion of MCF-7 cells across a Matrigel membrane was inhibited by 75% at 10 micro g/mL of pomegranate seed oil. Pomegranate seed oi also induced 54% apoptosis in MDA-MB-435 estrogen receptor negative metastatic human breast cancer cells. Fermented juice polyphenols resulted in 47% inhibition of cancerous lesion formation induced by the carcinogen 7,12-dimethylbenz[a]anthracene (DMBA) in a murine mammary gland organ culture.
Mouse mammary organ cultures were treated with pomegranate fermented juice polyphenols, a high-performance liquid chromatographic (HPLC) peak separated from fermented juice or pomegranate seed oil and on day 3, exposed to the carcinogen DMBA, and for 10 days treated with the putative pomegranate preparations. Fermented pomegranate juice resulted in a 42% reduction in the number of lesions compared with control, while the peak separated from the fermented juice and the pomegranate seed oil each resulted in an 87% reduction in number of tumorigenic lesions. The results suggested enhanced potential for the purified compound as well as pomegranate seed oil, both greater than pomegranate fermented juice polyphenols.
Toi et al. (2003) evaluated the anti-angiogenic potential of pomegranate polyphenols by measuring vascular endothelial growth factor (VEGF), interleukin-4 (IL-4), and migration inhibitory factor (MIF) in the conditioned media of MCF-7 or MDAMB- 231 human breast cancer cells, or immortalized normal human breast epithelial cells (MCF-10A). VEGF was strongly down-regulated in MCF-10A and MCF-7, and MIF up-regulated in MDA-MB-231, overall showing significant potential for down-regulation of angiogenesis by pomegranate fractions. These fractions further inhibited proliferation of human umbilical vein endothelial cells (HUVEC), myometrial, and amniotic fluid fibroblasts.
The effect of pomegranate extracts in combination with genistein was investigated on the growth rate and apoptosis induction in human breast cancer cells MCF-7. Both pomegranate extracts and genistein had significant dose- and time-dependent cytotoxic effects on MCF-7 cells. The inhibition and apoptosis induction were significantly higher in the combination treatments than in the single treatments with either agent isolated.
The aqueous PFE dosedependently inhibited NF-κB-dependent reporter gene expression in aggressive breast cancer phenotypes while decreasing RhoC and RhoA protein expression. Inhibition of motility and invasion by PFEs, coincident with suppressed RhoC and RhoA protein expression, suggests a role for these defined extracts in lowering the metastatic potential of aggressive breast cancer species.
Some doctors investigated the potential ability of punicic acid to affect growth of both an estrogen insensitive breast cancer cell line and an estrogen sensitive cell line developed from the MDA-MB-231 cells. Proliferation was inhibited 92 and 96% for MDA-MB-231 and MDA-ERalpha7 cells, respectively, compared to untreated cells by 40 micro M punicic acid.
Furthermore, punicic acid induced apoptosis in the MDA-MB-231 and MDAERalpha7 cells by 86 and 91%, respectively, compared to untreated control cells and disrupted cellular mitochondrial membrane potential. Punicic acid effects were partially blocked in the presence 20 micro M of the antioxidant tocotrienol or the PKC inhibitor bisindolymaleimide I in both the MDA-MB-231 and MDA-ERalpha7 cells. Thus, punicic acid, a component of the pomegranate seed oil, has breast cancer inhibitor properties that are dependent on lipid peroxidation and the PKC pathway.
Urolithin B was found to most effectively inhibit aromatase activity in a live cell assay. Proliferation assays also determined that urolithin B significantly inhibited testosterone-induced MCF-7 cell proliferation. Pomegranate seed linolenic acid isomers were evaluated as selective estrogen receptor modulators under in vitro conditions. These data provide evidence that pomegranate components exhibit selective estrogen receptor modulatory activity and suggested a potential for pomegranate-derived compounds for the prevention of estrogen-responsive breast cancers.
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