diallyl disulfide/neoplasms

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Diallyl disulfide (DADS) boosts TRAIL-Mediated apoptosis in colorectal cancer cells by inhibiting Bcl-2.

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Ever since several targeted agents were introduced a decade ago, progress in new therapeutic strategies for colorectal cancer (CRC) has been much slower than that for other cancers. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is widely known to induce cellular apoptosis in

Diallyl disulfide suppresses proliferation and induces apoptosis in human gastric cancer through Wnt-1 signaling pathway by up-regulation of miR-200b and miR-22.

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The purpose of this study was to identify a mechanism related to miRNA pathway which plays a role in the anti-tumor effects of Diallyl disulfide. Alterations in miRNA expression were observed in Diallyl disulfide-treated MGC-803 cells, including up-regulation of miR-200b and miR-22 expression.

Diallyl disulfide suppresses the growth of human colon tumor cell xenografts in athymic nude mice.

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The present studies examined the anti-proliferative effects of diallyl disulfide (DADS) on the growth of human colon tumor cell line, HCT-15, xenografts in 6-wk-old female NCr nu/nu mice with an initial body weight of 20-22 g. Intraperitoneal injection of 1 mg DADS thrice weekly reduced tumor volume

Effects of garlic components diallyl sulfide and diallyl disulfide on arylamine N-acetyltransferase activity in human bladder tumor cells.

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Diallyl sulfide (DAS) and diallyl disulfide (DADS) were used to determine viability and inhibition of arylamine N-acetyltransferase (NAT) activity in human bladder tumor cells. The NAT activity was measured by high performance liquid chromatography assaying for the amounts of

Histone deacetylases as targets for dietary cancer preventive agents: lessons learned with butyrate, diallyl disulfide, and sulforaphane.

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Cancer is a multi-factorial process involving genetic and epigenetic events which result in neoplastic transformation. Reversal of aberrant epigenetic events, including those that modulate the transcriptional activity of genes associated with various signaling pathways, holds the prospect of

Diallyl disulfide causes caspase-dependent apoptosis in human cancer cells through a Bax-triggered mitochondrial pathway.

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Diallyl disulfide (DADS), an important component of garlic (Allium sativum) derivative, has been demonstrated to exert a potential molecular target against human cancers. We investigated DADS-induced expressions of Apaf1, cystatin B, caspase-3 and FADD (fas-associated protein with death domain) in

Diallyl disulfide induces ERK phosphorylation and alters gene expression profiles in human colon tumor cells.

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Diallyl disulfide (DADS), a compound found in processed garlic, has been shown to arrest unsynchronized human colon tumor cells (HCT-15) in the G(2)/M phase of the cell cycle. The present studies were designed to examine whether this cell cycle block related to alterations in protein kinase C (PKC),

Molecular mechanism of diallyl disulfide in cell cycle arrest and apoptosis in HCT-116 colon cancer cells.

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Diallyl disulfide (DADS) is the most prevalent oil-soluble sulfur compound in garlic and inhibits cell proliferation in many cancer cell lines. Here we examined DADS cytotoxicity in a redox-mediated process, involving reactive oxygen species (ROS) production. In the present study, p53-independent

Diallyl disulfide induces Ca2+ mobilization in human colon cancer cell line SW480.

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Diallyl disulfide (DADS), one of the major organosulfur compounds of garlic, is recognized as a group of potential chemopreventive compounds. In this study, we examines the early signaling effects of DADS on human colorectal cancer cells SW480 loaded with Ca(2+)-sensitive dye fura-2. It was found

Erk is involved in the differentiation induced by diallyl disulfide in the human gastric cancer cell line MGC803.

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Diallyl disulfide (DADS) is a major constituent of garlic. Previously, we found that DADS both inhibited proliferation in human gastric cancer cells in vitro and in vivo, and induced G2/M arrest. In this study, we investigated whether this differentiation effect was induced by DADS in human gastric

Induction of apoptosis with diallyl disulfide in AGS gastric cancer cell line.

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OBJECTIVE Diallyl disulfide (DADS) is a major organosulfur compound derived from garlic. It has been reported that DADS is able to inhibit the proliferation of several tumor cells. In this study, the effect of DADS was investigated in terms of the proliferation of AGS, gastric adenocarcinoma cell

Garlic compound, diallyl disulfide induces cell cycle arrest in prostate cancer cell line PC-3.

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Prostate cancer is the most predominant cancer in men and related death rate increases every year. Till date, there is no effective therapy for androgen independent prostate cancer. Previous studies reported that aged garlic extract suppresses cancer growth. In the present study, diallyl disulfide

Effects of the garlic components diallyl sulfide and diallyl disulfide on arylamine N-acetyltransferase activity in human colon tumour cells.

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Diallyl sulfide (DAS) and diallyl disulfide (DADS), major components of garlic, were used to determine inhibition of arylamine N-acetyltransferase (NAT) activity in a human colon tumour (adenocarcinoma) cell line. Two assay systems were performed, one with cellular cytosols (9000g supernatant), the

Growth suppressing effect of garlic compound diallyl disulfide on prostate cancer cell line (PC-3) in vitro.

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Prostate cancer is the most predominant cancer in men and prostate cancer related death increases every year. Till date, there is no effective therapy other than androgen ablation therapy. At this stage, induction of apoptosis is considered as a better strategy to control cancer. Previous studies

Selective effects of diallyl disulfide, a sulfane sulfur precursor, in the liver and Ehrlich ascites tumor cells.

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The present in vivo studies demonstrated that diallyl disulfide (DADS), occurring in garlic, elevated hepatic sulfane sulfur level and activities of gamma-cystathionase and 3-mercaptopyruvate sulfotransferase in healthy mice but did not affect the hepatic glutathione level. DADS efficiently

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