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Anti-breast-Cancer Activity Exerted by β-Sitosterol-d-glucoside from Sweet Potato via Upregulation of MicroRNA-10a and via the PI3K-Akt Signaling Pathway.

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Breast cancer (BC) is a prominent source of cancer mortality in women throughout the world. β-Sitosterol-d-glucoside (β-SDG), a newly isolated phytosterol from sweet potato, possibly displays potent anticancer activity. However, the probable anticancer mechanisms involved are still unclear. This

Evaluation of β-Sitosterol Loaded PLGA and PEG-PLA Nanoparticles for Effective Treatment of Breast Cancer: Preparation, Physicochemical Characterization, and Antitumor Activity.

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β-Sitosterol (β-Sit) is a dietary phytosterol with demonstrated anticancer activity against a panel of cancers, but its poor solubility in water limits its bioavailability and therapeutic efficacy. In this study, poly(lactide-co-glycolic acid) (PLGA) and block copolymers of poly(ethylene

Inhibition of growth and stimulation of apoptosis by beta-sitosterol treatment of MDA-MB-231 human breast cancer cells in culture.

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Epidemiological and experimental studies have suggested a protective role of phytosterols (PS) in the development of some types of cancer such as colon and prostate cancer. No work has been reported on the role of PS in the development of breast cancer, the second leading cancer in woman. The

beta-Sitosterol activates Fas signaling in human breast cancer cells.

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beta-Sitosterol is the most abundant phytosterol. Phytosterols are enriched in legumes, oil seeds and unrefined plant oils as found in foods such as peanut butter, pistachios and sunflower seeds. beta-Sitosterol inhibits the growth of several specific types of tumor cells in vitro and decreases the

beta-Sitosterol enhances tamoxifen effectiveness on breast cancer cells by affecting ceramide metabolism.

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The objective of this study was to investigate the effects of the dietary phytosterol beta-sitosterol (SIT) and the antiestrogen drug tamoxifen (TAM) on cell growth and ceramide (CER) metabolism in MCF-7 and MDA-MB-231 human breast cancer cells. The MCF-7 and MDA-MB-231 cell lines were studied as

Beta-sitosterol, a plant sterol, induces apoptosis and activates key caspases in MDA-MB-231 human breast cancer cells.

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The objective of the present study was to evaluate the effect of beta-sitosterol, a plant sterol that induces apoptosis in breast cancer cells, on two pathways leading to apoptosis. These pathways are classified based on the localization of the initiated signal, extrinsic and intrinsic pathways.

beta-Sitosterol, beta-Sitosterol Glucoside, and a Mixture of beta-Sitosterol and beta-Sitosterol Glucoside Modulate the Growth of Estrogen-Responsive Breast Cancer Cells In Vitro and in Ovariectomized Athymic Mice.

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We hypothesized that the phytosterols beta-sitosterol (BSS), beta-sitosterol glucoside (BSSG), and Moducare (MC; BSS:BSSG = 99:1) could modulate the growth of estrogen-dependent human breast cancer cells in vitro and in vivo. The present study evaluated the estrogenic and antiestrogenic effects of

Beta-sitosterol sensitizes MDA-MB-231 cells to TRAIL-induced apoptosis.

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OBJECTIVE To investigate whether subtoxic concentration of beta-sitosterol (SITO) combined with TNF-related apoptosis-inducing ligand (TRAIL) induces apoptosis in TRAIL-resistant MDA-MB-231 breast cancer cells. METHODS Cell viability and growth were assessed by

Phytosterols and cholesterol in malignant and benign breast tumors.

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Tissue phytosterol and cholesterol levels in 10 benign and 8 malignant breast tumors were quantitated to reexamine the hypothesis that malignant tumors had distinctive phytosterol content. Phytosterols were present in 9 of 10 benign and 7 of 8 malignant breast tumors. Mean (+/- S.E.) cholesterol,

Effect of dietary intake of phytoestrogens on estrogen receptor status in premenopausal women with breast cancer.

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Although many dietary studies have focused on breast cancer risk, few have examined dietary influence on tumor characteristics such as estrogen receptor (ER) status. Because phytoestrogens may modulate hormone levels and ER expression, we analyzed ER status and phytoestrogen intake in a case-case

Beta-sitosterol induces anti-proliferation and apoptosis in human leukemic U937 cells through activation of caspase-3 and induction of Bax/Bcl-2 ratio.

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Beta-sitosterol is the main dietary phytosterol found in plants and has been shown to inhibit proliferation and induce apoptosis in human solid tumors such as colon and breast cancers. However, the mechanism by which beta-sitosterol induces apoptosis is not completely understood in leukemic cells.

Effect of phytosterols on cholesterol metabolism and MAP kinase in MDA-MB-231 human breast cancer cells.

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Epidemiological studies suggest that dietary phytosterols may offer protection form some types of cancer including breast cancer. In an attempt to investigate the mechanism by which phytosterols offer this protection, we investigated the effect of the two most common dietary phytosterols,

Dietary phytosterol inhibits the growth and metastasis of MDA-MB-231 human breast cancer cells grown in SCID mice.

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The objective of the present study was to investigate the effect of dietary phytosterols on the growth and metastasis of the human breast cancer MDA-MB-231 cell line xenografted in SCID mice. Two groups of animals were fed AIN-93G diet supplemented with 0.2% cholic acid and 2% sterol (cholesterol or

In vitro and in silico study of Aloe vera leaf extract against human breast cancer.

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Aloe vera leaf contains some bioactive compounds that have a strong binding affinity toward estrogen receptor as compared to standard drug tamoxifen. In this study, we have found that the IC₅₀ of Aloe vera leaf extract against breast cancer cell line (MCF-7) is 23 µg/mL which is much

The consumption of seaweed as a protective factor in the etiology of breast cancer.

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A review of the biological properties of seaweed is presented and the role of seaweed as a breast cancer anticarcinogen is suggested. Proposed mechanisms of action are: reduction of plasma cholesterol, binding of biliary steroids, inhibition of carcinogenic fecal flora, binding of pollutants,

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