quercetin/breast neoplasms

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Differential Effects of Quercetin and Two of Its Derivatives, Isorhamnetin and Isorhamnetin-3-glucuronide, in Inhibiting the Proliferation of Human Breast-Cancer MCF-7 Cells.

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Quercetin (Que) has consistently been reported to be useful cytotoxic compound in vivo and in vitro, but little is known on its metabolites. Here, we examined and compared the cytotoxic effects of Que and its water-soluble metabolites, isorhamnetin (IS) and isorhamnetin-3-glucuronide (I3G), in human

Dietary quercetin exacerbates the development of estrogen-induced breast tumors in female ACI rats.

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Phytoestrogens are plant compounds that structurally mimic the endogenous estrogen 17beta-estradiol (E(2)). Despite intense investigation, the net effect of phytoestrogen exposure on the breast remains unclear. The objective of the current study was to examine the effects of quercetin on

[Effects of quercetin on the proliferation and apoptosis in transplantation tumor of breast cancer in nude mice].

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OBJECTIVE To investigate the effects of quercetin on tumour growth, cell proliferation and apoptosis in transplantation tumor of breast cancer cell line MCF-7 in nude mice. METHODS MCF-7 cells were inoculated into the mammary fatty pad of nude mice to establish breast cancer model, then twenty-four

Quercetin conjugated with silica nanoparticles inhibits tumor growth in MCF-7 breast cancer cell lines.

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Quercetin is a plant polyphenol from the flavonoid group that plays a fundamental role in controlling homeostasis due to its potent antioxidant properties. However, quercetin has extremely low water solubility, which is a major challenge in drug absorption. In this study, we described a simple

Quercetin Is a Flavonoid Breast Cancer Resistance Protein Inhibitor with an Impact on the Oral Pharmacokinetics of Sulfasalazine in Rats.

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The potential inhibitory effect of quercetin, a major plant flavonol, on breast cancer resistance protein (BCRP) activity was investigated in this study. The presence of quercetin significantly increased the cellular accumulation and associated cytotoxicity of the BCRP substrate mitoxantrone in

Quercetin induces apoptosis and necroptosis in MCF-7 breast cancer cells.

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OBJECTIVE This study investigated the quercetin (Que) effects on growth of MCF-7 human cancer breast cell line and its cellular death mechanism. BACKGROUND Quercetin has been found to be very efficacious against many different types of cancer cells. However, the study is not sufficiently powered to

Quercetin, Siamois 1 and Siamois 2 induce apoptosis in human breast cancer MDA-mB-435 cells xenograft in vivo.

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We sought to investigate the apoptosis-inducing activities of quercetin, Siamois 1, and Siamois 2 against invasive estrogen-receptor negative MDA-MB 435 cells xenografted in athymic nude mice. This study clearly demonstrated that these compounds exhibited apoptosis-inducing activities in cell

The effect of quercetin on doxorubicin cytotoxicity in human breast cancer cells.

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Multidrug resistance has became the major obstacle to cancer chemotherapy. Recent studies suggest that quercetin could enhance the response of tumors to chemotherapy although the mechanism by which quercetin enhances the sensitivity of tumor cells to chemical drugs remains elusive. Therefore, in

Quercetin induces type-II estrogen-binding sites in estrogen-receptor-negative (MDA-MB231) and estrogen-receptor-positive (MCF-7) human breast-cancer cell lines.

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We show that flavonoids positively regulate type-II estrogen-binding site (type-II EBS) levels both in MCF-7 (ER-positive) and in MDA-MB231 (ER-negative) breast-cancer cells. Type-II EBS were measured by a whole-cell assay at 4 degrees C for 2.5 hr using [3H]-estradiol as tracer. In both cell lines

Regulation of mutual inhibitory activities between AMPK and Akt with quercetin in MCF-7 breast cancer cells.

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In lieu of elucidating bidirectional connecting mechanism between AMP-activated protein kinase (AMPK) and survival signal Akt we applied MCF-7 breast cancer cells to determine whether AMPK modulation alters Akt signals and vice versa. Suppression of Akt activities with a synthetic Akt inhibitor

Genistein and quercetin increase connexin43 and suppress growth of breast cancer cells.

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Connexin proteins form gap junctions, which permit direct exchange of cytoplasmic contents between neighboring cells. Evidence indicates that gap junctional intercellular communication (GJIC) is important for maintaining homeostasis and preventing cell transformation. Furthermore, connexins may have

Quercetin and epigallocatechin gallate inhibit glucose uptake and metabolism by breast cancer cells by an estrogen receptor-independent mechanism.

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In this study we characterized (3)H-2-deoxy-d-glucose ((3)H -DG) uptake by the estrogen receptor (ER)-positive MCF7 and the ER-negative MDA-MB-231 human breast cancer cell lines and investigated the effect of quercetin (QUE) and epigallocatechin gallate (EGCG) upon (3)H-DG uptake, glucose metabolism

Quercetin reversed MDR in breast cancer cells through down-regulating P-gp expression and eliminating cancer stem cells mediated by YB-1 nuclear translocation.

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Overexpression of P-glycoprotein (P-gp) plays an important role in mediating multidrug resistance (MDR), resulting in chemotherapy failure of tumor patients and enhancement of cancer stem cell characteristics. By preparing doxorubicin (Dox) resistant human breast cancer MCF-7 cells, here, we wanted

Quercetin Increase the Chemosensitivity of Breast Cancer Cells to Doxorubicin Via PTEN/Akt Pathway.

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Our previous study indicated that nontoxic doses of quercetin (Que) could increase the chemosensitivity of breast cancer cells to doxorubicin (Dox) although the mechanism still remains elusive. Therefore, in this study, we aimed to investigate the underlying mechanisms. MCF-7 cells and MCF-7/dox

Hyaluronic Acid Nanohydrogel Loaded With Quercetin Alone or in Combination to a Macrolide Derivative of Rapamycin RAD001 (Everolimus) as a New Treatment for Hormone-Responsive Human Breast Cancer.

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The aim of this study is based on the evaluation of anticancer, anti-inflammatory activities, and cellular uptake of hyaluronic acid nanohydrogel of quercetin tested alone and in combination to a macrolide derivative of rapamycin RAD001 (everolimus) on hormone-responsive breast cancer cell line

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