diallyl disulfide/cancer mamar

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[Diallyl disulfide inhibits invasion and metastasis of MCF-7 breast cancer cells in vitro by down-regulating p38 activity].

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OBJECTIVE To investigate the effect of diallyl disulfide (DADS) on invasion and metastasis of human breast cancer MCF-7 cells and explore the possible mechanism. METHODS MCF-7 cells treated with 100, 200, and 400 µmol/L of DADS for 24 h were examined for cell invasion and migration capacities using

Tristetraprolin: A novel target of diallyl disulfide that inhibits the progression of breast cancer.

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Diallyl disulfide (DADS), a volatile component of garlic oil, has various biological properties, including antioxidant, antiangiogenic and anticancer effects. The present study aimed to explore novel targets of DADS that may slow or stop the progression of breast cancer. First, xenograft tumor

Comparative effects of natural and synthetic diallyl disulfide on apoptosis of human breast-cancer MCF-7 cells.

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The apoptotic effects of natural (n-) and synthetic (s-) DADS (diallyl disulfide; 3,3'-thiobisprop-1-ene) on human breast-cancer MCF-7 cells were investigated in vitro. 5-Fu (5-fluorouracil) and CTX (cyclophosphamide; Cytoxan) were used as comparative control anticancer agents. After MCF-7 cells had

Diallyl disulfide inhibits growth and metastatic potential of human triple-negative breast cancer cells through inactivation of the β-catenin signaling pathway.

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METHODS Although diallyl disulfide (DADS), an important garlic (Allium sativum) derivative, has exhibited potential anticancer activity, the molecular mechanism of this activity remains unknown. In this study, we evaluated the antitumor activity of DADS in triple-negative breast cancer (TNBC) cell

Diallyl disulfide suppresses SRC/Ras/ERK signaling-mediated proliferation and metastasis in human breast cancer by up-regulating miR-34a.

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Diallyl disulfide (DADS) is one of the major volatile components of garlic oil. DADS has various biological properties, including anticancer, antiangiogenic, and antioxidant effects. However, the anticancer mechanisms of DADS in human breast cancer have not been elucidated, particularly in vivo. In

Growth inhibitory effects of diallyl disulfide on human breast cancer cell lines.

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Diallyl disulfide (DADS) is an oil-soluble organosulfur compound found in garlic. The effect of synthetic DADS on the growth of estrogen receptor (ER)-positive (KPL-1 and MCF-7) and -negative (MDA-MB-231 and MKL-F) human breast cancer cell lines was examined. In an in vitro MTT assay, regardless of

Diallyl Disulfide Inhibits Breast Cancer Stem Cell Progression and Glucose Metabolism by Targeting CD44/PKM2/AMPK Signaling.

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BACKGROUND It has been reported that diallyl disulfide (DADS) has anti-proliferative activity in many cancers. OBJECTIVE The purpose of this study was to investigate the functions of DADS and the underlying mechanisms of its effect in breast cancer stem cells (BCSCs). METHODS Mammosphere formation

RAGE receptor targeted bioconjuguate lipid nanoparticles of diallyl disulfide for improved apoptotic activity in triple negative breast cancer: in vitro studies.

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In the present study, we have demonstrated receptor for advanced glycation endproducts (RAGE) as a target for delivery of drugs specifically to triple negative breast cancer cells. We have prepared solid lipid nanoparticle formulation of cytotoxic agent di-allyl-disulfide (DADS) to overcome its

Diallyl disulfide-induced apoptosis in a breast-cancer cell line (MCF-7) may be caused by inhibition of histone deacetylation.

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The health benefits of garlic have been proven by epidemiological and experimental studies. Diallyl disulphide (DADS), the major organosulfur compound found in garlic oil, is known to lower the incidence of breast cancer both in vitro and in vivo. The studies reported here demonstrate that DADS

Apoptosis induced by diallyl disulfide in human breast cancer cell line MCF-7.

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OBJECTIVE To investigate the effect of diallyl disulfide (DADS), a component of garlic, on apoptosis in human mammary cancer cell line (MCF-7) and its mechanisms. METHODS Cytotoxicity was analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide assays. Morphology of apoptotic cells

The attenuation of early benzo(a)pyrene-induced carcinogenic insults by diallyl disulfide (DADS) in MCF-10A cells.

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Diallyl disulfide (DADS), a garlic organosulfur compound, has been researched as a cancer prevention agent; however, the role of DADS in the suppression of cancer initiation in nonneoplastic cells has not been elucidated. To evaluate DADS inhibition of early carcinogenic events, MCF-10A cells were

Differentiating and growth inhibitory effects of diallyl disulfide on cancer cells.

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Diallyl disulfide caused growth inhibition and differentiation of DS19 mouse erythroleukemic cells as judged by hemoglobin synthesis and induction of acetylcholinesterase activity. There was a 50% inhibition of cell division at about 0.25 mM diallyl disulfide which was much more effective than

Increased acetylation of histones induced by diallyl disulfide and structurally related molecules.

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In previous studies, diallyl disulfide induced differentiation in DS19 mouse erythroleukemic cells. A mechanism mediated by increased histone acetylation was investigated. Diallyl disulfide caused increased acetylation of H4 and H3 histones in DS19 cells and K562 human leukemic cells. Diallyl

Diallyl trisulfides, a natural histone deacetylase inhibitor, attenuate HIF-1α synthesis, and decreases breast cancer metastasis.

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Intratumoral hypoxia promotes the distant metastasis of cancer subclones. The clinical expression level of hypoxia-inducible factor-1α (HIF-1α) reflects the prognosis of a variety of cancers, especially breast cancer. Histone deacetylase (HDAC) inhibitors can target HIF-1α protein due to von

Diallyl disulfide inhibits TNFα-induced CCL2 release by MDA-MB-231 cells.

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Monocyte chemotactic protein-1 (MCP-1/CCL2) is released by tumor tissues, serving as a potent chemokine enabling directional homing of mononuclear cells to tumor tissue, which subsequently differentiate into tumor-associated macrophages (TAMs) via TGFβ1 signaling. TAMs readily invade tumor tissue

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