ouabain/neoplasms

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Enhancement of recovery of chemical carcinogen-induced ouabain-resistant mutants in Chinese hamster cells by the tumor-promoting agent, 12-o-tetradecanoyl-phorbol-13-acetate.

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The effects of a tumor-promoting agent on the frequency of mutation to ouabain resistance and survival of Chinese hamster cells treated with a chemical carcinogen have been investigated. 12-O-Tetradecanoyl-phorbol-13-acetate (TPA) significantly enhanced the mutation frequency induced by the

The effect of SCF and ouabain on small intestinal motility dysfunction induced by gastric cancer peritoneal metastasis.

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The interstitial cells of Cajal (ICCs) play an important role in maintaining the normal function of gastrointestinal dynamics. In our previous study, we reported that, in advanced gastric cancer, the frequency of bowel movement is always reduced, due in part to the decreased number of ICCs. To

Effects of valinomycin, ouabain, and potassium on glycolysis and intracellular pH of Ehrlich ascites tumor cells.

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Both valinomycin and ouabain block reaccumulation of K(+) by Ehrlich ascites tumor cells depleted of K(+) and cause loss of K(+) from high-K(+) cells. Glucose largely reverses the effect of valinomycin and to a lesser extent that of ouabain.In cells depleted of K(+), glucose utilization and lactate

Digoxin and ouabain induce P-glycoprotein by activating calmodulin kinase II and hypoxia-inducible factor-1alpha in human colon cancer cells.

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Digoxin and ouabain are cardioactive glycosides, which inhibit the Na+/K+-ATPase pump and in this way they increase the intracellular concentration of cytosolic calcium ([Ca2+](i)). They are also strong inducers of the P-glycoprotein (Pgp), a transmembrane transporter which extrudes several drugs,

Ouabain suppresses the migratory behavior of lung cancer cells.

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The migratory capability of cancer cells is one of the most important hallmarks reflecting metastatic potential. Ouabain, an endogenous cardiac glycoside produced by the adrenal gland, has been previously reported to have anti-tumor activities; however, its role in the regulation of cancer cell

Ouabain downregulates Mcl-1 and sensitizes lung cancer cells to TRAIL-induced apoptosis.

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Resistance to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a prerequisite for cancer progression, and TRAIL resistance is prevalent in lung cancer. Ouabain, a recently identified human hormone, has shown therapeutic promise by potentiating the apoptotic response of metastatic

Effects of ouabain on NIH/3T3 cells transformed with retroviral oncogenes and on human tumor cell lines.

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Both murine and human cell lines transformed by the v-Ki-ras gene have been shown to be much more sensitive to the toxic effects of the cardiac glycoside ouabain than their respective controls. This differential toxicity has previously been used in the isolation of flat revertant clones from

Ouabain targets the Na+/K+-ATPase α3 isoform to inhibit cancer cell proliferation and induce apoptosis.

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Ouabain has been used for the treatment of heart failure and atrial fibrillation. Its potential anticancer effect has also attracted great interest. The aim of the present study was to evaluate the anticancer effect of ouabain and investigate its molecular target. The effects of ouabain on the

Antiproliferative activity of derivatives of ouabain, digoxin and proscillaridin A in human MCF-7 and MDA-MB-231 breast cancer cells.

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Three derivatives of ouabain, digoxin and proscillaridin A containing the carboxylic group instead of the lactone moiety were synthesized and examined for cytotoxicity in human breast cancer cells. Evaluation of the cytotoxicity of these compounds employing an MTT assay and inhibition of

Ouabain impairs cancer metabolism and activates AMPK-Src signaling pathway in human cancer cell lines.

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In addition to the well-known cardiotonic effects, cardiac glycosides (CGs) produce potent anticancer effects with various molecular mechanisms. We previously show that ouabain induces autophagic cell death in human lung cancer cells by regulating AMPK-mediated mTOR and Src-mediated ERK1/2 signaling

Investigation of ouabain-induced anticancer effect in human androgen-independent prostate cancer PC-3 cells.

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To determine the therapeutic potential of cardiac glycosides in androgen-independent prostate cancer, we examined ouabain-induced cytotoxic effect as well as the signaling pathways in PC-3 cells. Ouabain induced a time- and concentration-dependent cytotoxicity using mitochondrial MTT reduction

Cardiac glycoside ouabain induces autophagic cell death in non-small cell lung cancer cells via a JNK-dependent decrease of Bcl-2.

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Cardiac glycosides are Na/K-ATPase inhibitors, clinically used for congestive heart failure and cardiac arrhythmias. Epidemiological studies have reported that patients on cardiac glycosides treatment are protected from some types of cancers. This evidence together with the demonstration that

Inhibition of DNA topoisomerases I and II, and growth inhibition of breast cancer MCF-7 cells by ouabain, digoxin and proscillaridin A.

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We evaluated the cytotoxicity and underlying mechanisms of cardiac glycosides, including digoxin, ouabain and proscillaridin A, on the proliferation of breast cancer MCF-7 cells. In terms of inhibition of cell proliferation of MCF-7 cells, the compounds rank in the order proscillaridin

The antiproliferative effects of ouabain and everolimus on adrenocortical tumor cells.

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Ouabain is a cardiotonic steroid obtained from Strophanthus. Recently its role as antiproliferative agent has been investigated in tumor cells. Everolimus is a derivative of rapamycin and acts as a signal transduction inhibitor. Adrenocortical carcinoma is a rare cancer, with poor prognosis. This

Sodium/potassium ATPase (Na+, K+-ATPase) and ouabain/related cardiac glycosides: A new paradigm for development of anti- breast cancer drugs?

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Prolonged exposure to 17beta-estradiol (E2) is a key etiological factor for human breast cancer. The biological effects and carcinogenic effects of E2 are mediated via estrogen receptors (ERs), ERalpha and ERbeta. Anti-estrogens, e.g. tamoxifen, and aromatase inhibitors have been used to treat

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