anthraquinone/cancro

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Anthraquinones sensitize tumor cells to arsenic cytotoxicity in vitro and in vivo via reactive oxygen species-mediated dual regulation of apoptosis.

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Cellular oxidation/reduction state affects the cytotoxicity of a number of chemotherapeutic agents, including arsenic trioxide. Reactive oxygen species (ROS), the major intracellular oxidants, may be a determinant of cellular susceptibility to arsenic. Our previous studies showed that a

Silica nanoparticles doped with anthraquinone for lung cancer phototherapy.

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In the present study, SiO2 nanoparticles functionalized with 3-(2-aminoethylamino)propyl group (SiNP-AAP) were used, for the first time, to covalently bond rose bengal (SiNP-AAP-RB) or 9,10-anthraquinone-2-carboxylic acid (SiNP-AAP-OCAq). The functionalized SiNP were characterized by: Scanning

The novel anthraquinone derivative IMP1338 induces death of human cancer cells by p53-independent S and G2/M cell cycle arrest.

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To identify novel small molecules that induce selective cancer cell death, we screened a chemical library containing 1040 compounds in HT29 colon cancer and CCD18-Co normal colon cells, using a phenotypic cell-based viability assay system with the Cell Counting Kit-8 (CCK-8). We discovered a novel

Photochemotherapy using natural anthraquinones: Rubiadin and Soranjidiol sensitize human cancer cell to die by apoptosis.

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Over the past decade the science has studied synthetic photosensitizers used in photodynamic therapy (PDT) or photochemotherapy as anticancer candidates. In this context, compounds extracted from vegetable species present interesting potential in the cancer field. In our laboratory, we studied

Separation methods for anthraquinone related anti-cancer drugs.

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The quinoid anthracycline-related anti-cancer agents represent an important group of anti-tumour drugs with a wide spectrum of activity. We review here some of the separation techniques used for the analysis of anthracyclines and related compounds. In this review we have covered a range of compounds

Cytotoxicity of anthraquinones from the roots of Pentas schimperi towards multi-factorial drug-resistant cancer cells.

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BACKGROUND Multidrug resistance in cancer represents a major problem in chemotherapy. The present study was designed to assess the cytotoxicity of anthraquinones from Pentas schimperi, namely damnacanthal (1), damnacanthol (2), 3-hydroxy-2-hydroxymethyl anthraquinone (3) and schimperiquinone B (4)

Novel Anthraquinone Compounds Induce Cancer Cell Death through Paraptosis.

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Novel anthraquinone compounds that induce ER stress and paraptosis-like cell death were designed and synthesized. Compound 4a is the first organic micromolecule to kill tumor cells by only paraptosis, and its mechanism of action has been further explored. Paraptosis does not appear to involve

L-proline analogues of anthraquinone-2-carboxylic acid: cytotoxic activity in breast cancer MCF-7 cells and inhibitory activity against topoisomerase I and II.

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A series of proline analogues of anthraquinone-2-carboxylic acid (1-3) were synthesized and evaluated for cytotoxic activity in the cultured breast cancer MCF-7 cells. The concentrations of 1, 2 and 3 needed to inhibit [3H]thymidine incorporation into DNA by 50% (IC50) were found to be 107 +/- 6

The anthraquinone derivative Emodin inhibits angiogenesis and metastasis through downregulating Runx2 activity in breast cancer.

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Emodin (EMD) is an anthraquinone derivative extracted from the root and rhizome of Rheum palmatum L. which exhibits a range of activities, including anti-bacterial, antitumor, diuretic and vasorelaxant effects. The ability to inhibit metastasis and angiogenesis was shown in previous pharmacological

Synthesis and biological evaluation of anthraquinone derivatives as allosteric phosphoglycerate mutase 1 inhibitors for cancer treatment.

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Phosphoglycerate mutase 1 (PGAM1) coordinates glycolysis, pentose phosphate pathway, and serine synthesis to promote tumor growth through the regulation of its substrate 3-phosphoglycerate (3 PG) and product 2-phosphoglycerate (2 PG). Herein, based on our previously reported PGAM1 inhibitor

New approaches of PARP-1 inhibitors in human lung cancer cells and cancer stem-like cells by some selected anthraquinone-derived small molecules.

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Poly (ADP-ribose) polymerase-1 (PARP-1) and telomerase, as well as DNA damage response pathways are targets for anticancer drug development, and specific inhibitors are currently under clinical investigation. The purpose of this work is to evaluate anticancer activities of anthraquinone-derived

DNA sequence preferences for the anti-cancer drug mitoxanthrone and related anthraquinones revealed by DNase I footprinting.

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The interaction has been studied of several anthraquinone-based intercalating drugs, including the anti-cancer agent mitoxantrone, with defined sites of DNA. A 160 base pair DNA sequence from tyrT was employed for footprinting with DNase I. The anthraquinones had aminoalkylamino substituents in

[Impressive picture of a melanosis coli after chronic anthraquinone laxative use--is there an increased risk for colorectal cancer?].

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We report the case of a 74-year-old female with an extreme picture of melanosis coli of the whole colon after chronic use of anthraquinone laxatives for the treatment of constipation over many decades. Endoscopic work-up revealed an impressive deep black pigmentation of the whole colon mucosa which

Molecular complexes of some anthraquinone anti-cancer drugs: experimental and computational study.

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It is known that anti-cancer drugs target DNA in the cell. The mechanism of interaction of anti-cancer drugs with DNA is not fully understood. It is thought that the forces of interaction have some contribution from charge-transfer (CT) binding. The ability of some anthraquinones (AQs) anti-cancer

Novel anthraquinone derivatives: synthesis via click chemistry approach and their induction of apoptosis in BGC gastric cancer cells via reactive oxygen species (ROS)-dependent mitochondrial pathway.

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Three water soluble anthraquinone derivatives were designed and synthesized employing click chemistry to prepare novel and potent antitumor drugs. An MTT assay indicated that all compounds had significant inhibitory activity against BGC gastric cancer cells in vitro. Apoptosis induced by these

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