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Page 1 from 41 results
Ryanodine receptor expression correlates with tumor grade in breast cancer.
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Ryanodine receptors (RyRs) have been previously implicated in the proliferation of human T-lymphocytes and melanocytes as well as in the motility of astrocytes. We have examined RyR expression in 57 ductal, human breast cancer specimens, by immunohistochemistry. Moderate to high RyR immunostaining
Neferine induces autophagy-dependent cell death in apoptosis-resistant cancers via ryanodine receptor and Ca2+-dependent mechanism.
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Resistance of cancer cells to chemotherapy is a significant clinical concern and mechanisms regulating cell death in cancer therapy, including apoptosis, autophagy or necrosis, have been extensively investigated over the last decade. Accordingly, the identification of medicinal compounds against
The effects of ryanodine receptor (RYR1) mutation on natural killer cell cytotoxicity, plasma cytokines and stress hormones during acute intermittent exercise in pigs.
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Stress susceptibility has been mapped to a single recessive gene, the ryanodine receptor 1 (RYR1) gene or halothane (Hal) gene. Homozygous (Hal(nn)), mutated pigs are sensitive to halothane and susceptible to Porcine Stress Syndrome (PSS). Previous studies have shown that stress-susceptible RYR1
[Developments in cancer management by innovative genomics. 2006 report of the National Cancer Consortium].
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Research on developing molecular diagnostics for hereditary cancers resulted in establishing diagnostic services for familiar polyposis and non-polyposis patients (mutation determination of APC, MYH, STK11, SMAD4, MLH1, MSH2). In familiar testicular cancers the role of gr/gr gene on Y chromosome was
Differential Free Intracellular Calcium Release by Class II Antiarrhythmics in Cancer Cell Lines.
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Class II antiarrhythmics or β-blockers are antisympathetic nervous system agents that act by blocking β-adrenoceptors. Despite their common clinical use, little is known about the effects of β-blockers on free intracellular calcium (Ca2+i), an important
MTOR-independent autophagy induced by interrupted endoplasmic reticulum-mitochondrial Ca2+ communication: a dead end in cancer cells.
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The interruption of endoplasmic reticulum (ER)-mitochondrial Ca2+ communication induces a bioenergetic crisis characterized by an increase of MTOR-independent AMPK-dependent macroautophagic/autophagic flux, which is not sufficient to reestablish the metabolic and energetic homeostasis in cancer
Vascular activity of two silicon compounds, ALIS 409 and ALIS 421, novel multidrug-resistance reverting agents in cancer cells.
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OBJECTIVE
The aim of this study was to investigate the effects of two novel multidrug-resistance reverting agents, ALIS 409 [1,3-dimethyl-1,3-p-fluorophenyl-1,3(3-morfolinopropyl)-1,3-disiloxan dihydrochloride] and ALIS 421
Panaxydol, a component of Panax ginseng, induces apoptosis in cancer cells through EGFR activation and ER stress and inhibits tumor growth in mouse models.
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We reported previously that panaxydol, a component of Panax ginseng roots, induced mitochondria-mediated apoptosis preferentially in transformed cells. This study demonstrates that EGFR activation and the resulting ER stress mediate panaxydol-induced apoptosis, and that panaxydol suppresses in vivo
A novel mechanism underlying phytate-mediated biological action-phytate hydrolysates induce intracellular calcium signaling by a Gαq protein-coupled receptor and phospholipase C-dependent mechanism in colorectal cancer cells.
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Phytate (inositol hexa-phosphate, IP6) possesses multiple biological functions including anticancer activity. IP6 is converted to inositol di-, tri-, and tetra-phosphates (IP2, IP3, and IP4) by phytase in large intestinal microbes; however, their contribution to the IP6-mediated functions has not
Cytotoxic effects and apoptotic signalling mechanisms of the sesquiterpenoid euplotin C, a secondary metabolite of the marine ciliate Euplotes crassus, in tumour cells.
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Most antitumour agents with cytotoxic properties induce apoptosis. The lipophilic compound euplotin C, isolated from the ciliate Euplotes crassus, is toxic to a number of different opportunistic or pathogenic microorganisms, although its mechanism of action is currently unknown. We report here that
Epigallocatechin-3-gallate mobilizes intracellular Ca 2+ in prostate cancer cells through combined Ca 2+ entry and Ca 2+-induced Ca 2+ release
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Aims: To elucidate the mechanism by which (-)-epigallocatechin-3-gallate (EGCG) mediates intracellular Ca increase in androgen-independent prostate cancer (PCa) cells.
Main methods:
Tumor necrosis factor activation of vagal afferent terminal calcium is blocked by cannabinoids.
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The early proinflammatory cytokine tumor necrosis factor (TNF) is released in significant quantities by the activated immune system in response to infection, leukemia, autoimmune disorders, and radiation sickness. Nausea, emesis, and anorexia are common features of these disorders. TNF action on
Mitochondrial Hsp90s suppress calcium-mediated stress signals propagating from mitochondria to the ER in cancer cells.
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BACKGROUND
Resistance to cell death in the presence of stressful stimuli is one of the hallmarks of cancer cells acquired during multistep tumorigenesis, and knowledge of the molecular mechanism of stress adaptation can be exploited to develop cancer-selective therapeutics. Mitochondria and the
Dantrolene Attenuates Cardiotoxicity of Doxorubicin Without Reducing its Antitumor Efficacy in a Breast Cancer Model.
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Dysregulation of calcium homeostasis is a major mechanism of doxorubicin (DOX)-induced cardiotoxicity. Treatment with DOX causes activation of sarcoplasmic reticulum (SR) ryanodine receptor (RYR) and rapid release of Ca2+ in the cytoplasm resulting in depression of myocardial function.
Acquired short QT syndrome in a cancer patient treated with Toad.
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Although drug-induced short QT syndrome (SQTS) has been recognized, we currently report the first acquired SQTS case induced by bufotalinin (toad, an antineoplastic drug), which is a traditional Chinese folk prescription. It has cross reaction with digoxin and affects the Na+
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