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disulfide/рак

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Страна 1 од 1946 резултати

Disulfide linkage: a potent strategy in tumor-targeting drug discovery.

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Targeted drug delivery has attracted much attention in improving the curative effect of existing chemotherapy drugs, and many published studies have suggested the disulfide linkage for key unit in constructing a targeting conjugate. An appropriate disulfide bond,through which cytotoxic agents and

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

Biotinylated transferrin/avidin/biotinylated disulfide containing PEI bioconjugates mediated p53 gene delivery system for tumor targeted transfection.

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As mutation and dysfunction of p53 gene could induce most of human cancers, the p53 tumor suppressor gene was used to replace them and recover their normal functions in cancer cells. In this paper, biotinylated transferrin/avidin/biotinylated disulfide containing PEI bioconjugates (TABP-SS) mediated

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

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

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

Disulfide cross-linked polyurethane micelles as a reduction-triggered drug delivery system for cancer therapy.

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Nanoscale carriers that stably load drugs in blood circulation and release the payloads in desirable sites in response to a specific trigger are of great interest for smart drug delivery systems. For this purpose, a novel type of disulfide core cross-linked micelles, which are facilely fabricated by

Two-Photon Fluorescent Molybdenum Disulfide Dots for Targeted Prostate Cancer Imaging in the Biological II Window.

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Molybdenum disulfide (MoS2) quantum dots (QDs) derived from this two-dimensional (2D) transition metal dichalcogenide are emerging zero-dimensional materials that possess very good optical properties. Bioimaging using light in the biological II window (950-1350 nm) is a next-generation approach that

Disulfide bond-disrupting agents activate the tumor necrosis family-related apoptosis-inducing ligand/death receptor 5 pathway.

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Disulfide bond-disrupting agents (DDAs) are a new chemical class of agents recently shown to have activity against breast tumors in animal models. Blockade of tumor growth is associated with downregulation of EGFR, HER2, and HER3 and reduced Akt phosphorylation, as well as the induction of

Disulfide bond disrupting agents activate the unfolded protein response in EGFR- and HER2-positive breast tumor cells.

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Many breast cancer deaths result from tumors acquiring resistance to available therapies. Thus, new therapeutic agents are needed for targeting drug-resistant breast cancers. Drug-refractory breast cancers include HER2+ tumors that have acquired resistance to HER2-targeted antibodies and kinase

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
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