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cardiolipin/kræft
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A Novel Arylurea Fatty Acid That Targets the Mitochondrion and Depletes Cardiolipin To Promote Killing of Breast Cancer Cells.
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Cancer cell mitochondria are promising anticancer drug targets because they control cell death and are structurally and functionally different from normal cell mitochondria. We synthesized arylurea fatty acids and found that the analogue
In-vitro and in-vivo anti-cancer activity of a novel gemcitabine-cardiolipin conjugate.
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Our objectives were to study the biological activity of a novel gemcitabine-cardiolipin conjugate (NEO6002) and compare that with gemcitabine. Cytotoxicity in vitro was determined against several gemcitabine-sensitive parental and gemcitabine-resistant cancer cell lines using the sulforhodamine B
The Cytotoxic Action of Cytochrome C/Cardiolipin Nanocomplex (Cyt-CL) on Cancer Cells in Culture.
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The effect of existing anti-cancer therapies is based mainly on the stimulation of apoptosis in cancer cells. Here, we have demonstrated the ability of a catalytically-reactive nanoparticle-based complex of cytochrome c with cardiolipin (Cyt-CL) to induce the apoptosis and killing of cancer cells in
Regulation of hepatic cardiolipin metabolism by TNFα: Implication in cancer cachexia.
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Cardiolipin (CL) content accumulation leads to an increase in energy wasting in liver mitochondria in a rat model of cancer cachexia in which tumor necrosis factor alpha (TNFα) is highly expressed. In this study we investigated the mechanisms involved in liver mitochondria CL accumulation in cancer
Role of mitochondria and cardiolipins in growth inhibition of breast cancer cells by retinoic acid.
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Serum cardiolipin antibodies in cancer patients with thromboembolic events.
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This study was undertaken to investigate a possible association of anticardiolipin antibodies (ACLAs) in cancer patients with thromboembolic events. Twenty-five patients with solid tumors complicated with acute thrombosis, 36 cancer patients without any thrombotic events, and a group of 20 healthy
A new pyrrole based small molecule from Tinospora cordifolia induces apoptosis in MDA-MB-231 breast cancer cells via ROS mediated mitochondrial damage and restoration of p53 activity.
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Approximately 15% of globally diagnosed breast cancers are designated as triple negative breast cancer (TNBC). In this study, we investigated the effect of the natural compound, Bis(2- ethyl hexyl) 1H-pyrrole-3,4-dicarboxylate (TCCP), purified from Tinospora cordifolia on MDA-MB-231, a TNBC cell
Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) induced mitochondrial pathway to apoptosis and caspase activation is potentiated by phospholipid scramblase-3.
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Tumor Necrosis Factor (TNF)-Related Apoptosis-Inducing Ligand (TRAIL) initiate pathways of cell death in which caspase activation is mediated either directly (without mitochondrial amplification), or indirectly via the release of apoptogenic factors from mitochondria. Phospholipid scramblases (PLS)
Stimulation of brown adipose tissue activity in tumor-bearing rats.
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Despite anorexia, cancer development is frequently accompanied by an increase of energy expenditure. Considering the pivotal role played by brown adipose tissue (BAT) in the energy metabolism of small mammals, we investigated the functional and compositional modification in BAT of anorexic
[Biosynthesis of cardiolipin in the rat hepatoma 27 and Jensen sarcoma].
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The localization of cardiolipin biosynthesis in rat hepatoma 27 and Jensen sarcoma cells was investigated. In both tumors cardiolipin was found to be synthesized only in the mitochondria as is the case in normal rat liver. It is concluded that the occurrence of cardiolipin in the microsomes of the
Cholesterol, cardiolipin, and mitochondria permeabilisation.
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Apoptosis is a form of programmed cell death required for the development and for the proper functioning of multicellular organisms. It is defined by a combination of morphological and biochemical modifications that result from the activation of a family of proteases called caspases. Several
Identification of lipids associated with the ability of tumor cells to resist humoral immune attack.
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Certain metabolic inhibitors or chemotherapeutic agents that increase the susceptibility of line-1 or line-10 guinea pig hepatoma cells to humoral immune attack were studied for their effects on the ability of the cells to synthesize lipids. A direct correlation was found between the drug-induced
Plasma membrane and intracellular lipid synthesis in tumor cells rendered resistant to humoral immune killing after treatment with hormones.
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Line-10 hepatoma cells from Sewall Wright guinea pigs are sensitive to killing by antibody plus human complement. Hormones that decrease the sensitivity of the cells to antibody-complement-mediated killing (insulin and hydrocortisone) were examined for their effects on the ability of the cells to
Plasma membrane and intracellular lipid synthesis in tumor cells rendered sensitive to humoral immune killing after treatment with metabolic inhibitors.
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Line 10 guinea pigs hepatoma cells are resistant to killing by antibody and guinea pig complement. Metabolic inhibitors (adriamycin and actinomycin D) that increase the sensitivity of the cells to antibody-complement (C) killing were examined for their effects on the ability of the cells to
Decreased mitochondrial function in quiescent cells isolated from multicellular tumor spheroids.
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Cells in the inner region of multicellular spheroids markedly reduce their oxygen consumption rate, presumably in response to their stressful microenvironment. To determine the mechanism behind this metabolic adaptation, we have investigated relative mitochondrial mass and mitochondrial function in
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