Naringenin and 17β‐estradiol coadministration prevents hormone‐induced human cancer cell growth

  title={Naringenin and 17$\beta$‐estradiol coadministration prevents hormone‐induced human cancer cell growth},
  author={Pamela Bulzomi and Alessandro Bolli and Paola Galluzzo and Stefano Leone and Filippo Acconcia and Maria Marino},
  journal={IUBMB Life},
Flavonoids have been described as health‐promoting, disease‐preventing dietary components. In vivo and in vitro experiments also support a protective effect of flavonoids to reduce the incidence of certain hormone‐responsive cancers. In particular, our previous results indicate that the flavanone naringenin (Nar), decoupling estrogen receptor α (ERα) action mechanisms, drives cancer cells to apoptosis. Because these studies were conducted in the absence of the endogenous hormone 17β‐estradiol… 

The naringenin‐induced proapoptotic effect in breast cancer cell lines holds out against a high bisphenol a background

As a whole, Nar maintains its proapoptotic effects even in the presence of the food contaminant BPA, thus, enlarging the chemopreventive potential of this flavanone.

Naringenin modulates skeletal muscle differentiation via estrogen receptor α and β signal pathway regulation

Data reported here strongly sustain that although Nar action mechanisms include the impairment of ERα signals which drive muscle cells to differentiation, the effects triggered by Nar in the presence of ERβ could balance this negative effect avoiding the toxic effects produced by oxidative stress.

Xenoestrogens Alter Estrogen Receptor (ER) α Intracellular Levels

Data demonstrate that ERα intracellular concentration is an important target through which EDs hamper the hormonal milieu of E2 target cells driving cells to different outcomes or mimicking E2 even in the absence of the hormone.

Beyond the Antioxidant Activity of Dietary Polyphenols in Cancer: the Modulation of Estrogen Receptors (ERs) Signaling

The role and effects of food-contained polyphenols in hormone-related cancers will be reviewed, mainly focusing on the differentpolyphenols’ mechanisms of action with particular attention on their estrogen receptor-based effects, and on the consequences of such processes on tumor progression and development.

Xenoestrogen regulation of ERα/ERβ balance in hormone-associated cancers

Targeting inflammatory pathways by flavonoids for prevention and treatment of cancer.

Various flavones, flavanones, Flavonols, isoflavones, anthocyanins, and chalcones derived from fruits, vegetables, legumes, spices, and nuts that can suppress the proinflammatory cell signaling pathways and thus can prevent and even treat the cancer.



Mechanisms of Naringenin‐induced Apoptotic Cascade in Cancer Cells: Involvement of Estrogen Receptor a and ß Signalling

Findings indicate new steps in the mechanism underlying ER‐dependent anti‐proliferative effects of Nar suggesting new potential chemopreventive actions of flavonoids on cancer growth.

Nutritional Flavonoids Modulate Estrogen Receptor α Signaling

Flavonoids act as E2 mimetic on ERα transcriptional activity, whereas they impair the activation of rapid signaling pathways committed to E2‐induced proliferation, indicating that the antimitogenic effects of flavonoids are transduced by modulating ERα‐mediated rapid signaling.

Laccase treatment impairs bisphenol A‐induced cancer cell proliferation affecting estrogen receptor α‐dependent rapid signals

Laccase appears to impair BPA action(s), representing an invaluable bioremediation enzyme that participates to BPA‐induced cytotoxicity.

The nutritional flavanone naringenin triggers antiestrogenic effects by regulating estrogen receptor alpha-palmitoylation.

New ER-dependent mechanisms on the root of antiproliferative and antiestrogenic effects of Nar are highlighted, including the different modulation of ERalpha palmitoylation exerted by different ligands represents a pivotal mechanism that drives cancer cell to proliferation or apoptosis.

Survival versus apoptotic 17β‐estradiol effect: Role of ERα and ERβ activated non‐genomic signaling

The ability of ERβ isoform to activate specific signal transduction pathways starting from plasma membrane that may justify the effect of E2 in inducing cell proliferation or apoptosis in cancer cells is demonstrated.

Phytoestrogens Induce Differential Estrogen Receptor Alpha- or Beta-Mediated Responses in Transfected Breast Cancer Cells

This transfection assay provides an excellent model to evaluate the activation of ERα and ERβ by different phytoestrogens in a breast cancer context and can be used as a screening bioassay tool to evaluation the estrogenic activity of extracts of herbs and foods.

Changes in gene expressions elicited by physiological concentrations of genistein on human endometrial cancer cells

Results indicate that at physiological concentrations, genistein is able to elicit pleiotropic effects on a variety of pathways believed to be involved in tumorigenesis.

Estrogen receptor β inhibits 17β-estradiol-stimulated proliferation of the breast cancer cell line T47D

It is shown that induced expression of ERβ in the breast cancer cell line T47D reduces 17β-estradiol-stimulated proliferation when expression ofERβ mRNA equals that of ERα, implying that ERβ-specific ligands may reduce proliferation of ER-positive breast cancer cells through actions on the G1 phase cell-cycle machinery.