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butyric acid/kræft
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Gamma-amino butyric acid (GABA) prevents the induction of nicotinic receptor-regulated signaling by chronic ethanol in pancreatic cancer cells and normal duct epithelia.
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Pancreatic cancer has a high mortality rate and alcoholism is a risk factor independent of smoking. We have shown that nicotinic acetylcholine receptors (nAChR) regulate pancreatic ductal epithelia and pancreatic ductal adenocarcinoma (PDAC) cells in an autocrine fashion by stimulating their
Role of butyric acid and its derivatives in the treatment of colorectal cancer and hemoglobinopathies.
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Butyric acid, a short chain fatty acid (SCFA), is a natural component of the animal metabolism. Physiological concentrations induce multiple and reversible biological effects. They concern regulatory mechanisms of gene expression conducing to promote markers of cell differentiation, apoptosis and
A survey on anticancer effects of artemisinin, iron, miconazole, and butyric acid on 5637 (bladder cancer) and 4T1 (Breast cancer) cell lines.
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BACKGROUND
Anticancer properties of artemisinin and its derivatives have been shown in many experiments.
OBJECTIVE
Addition of butyric acid, miconazole, and iron to this traditional drug has been done in order to enhance its anticancer potency.
METHODS
Cell lines 5637 and 4T1, were cultivated and
Erratum to Design, Synthesis and Biological Evaluation of a Phenyl Butyric Acid Derivative, N-(4-chlorophenyl)-4- phenylbutanamide: A HDAC6 Inhibitor with Anti-proliferative Activity on Cervix Cancer and Leukemia Cells.
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Due to an oversight one of the author's name was published wrong in the article entitled "Design, Synthesis and Biological Evaluation of a Phenyl Butyric Acid Derivative, N-(4-chlorophenyl)-4- phenylbutanamide: A HDAC6 Inhibitor with Anti-proliferative Activity on Cervix Cancer and Leukemia
Derivatives of butyric acid as potential anti-neoplastic agents.
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A novel derivative of butyric acid, pivalyloxymethyl butyrate (AN-9) has been shown, in vitro, to: (a) induce cytodifferentiation and inhibit the proliferation of leukemic cells; (b) inhibit the growth and formation of Lewis lung carcinoma colonies in semi-solid agar. AN-9 affect cells at about
Antiproliferative effect of alkylglycerols as vehicles of butyric acid on colon cancer cells.
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The anticarcinogenic activity of synthetic 1-O-octadecyl-2,3-dibutyroilglycerol (D-SCAKG) in tumor-cell line of colonocytes (SW620) was performed. The effect of the previously digested D-SCAKG under in vitro intestinal conditions was compared to the bioactivity of non-digested D-SCAKG.
Synthesis of L-2,4-diamino[4-11C]butyric acid and its use in some in vitro and in vivo tumour models.
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L-2,4-Diamino[4-11C]butyric acid (DAB) was synthesized by an enzyme catalysed carrier added (0.1 micromol KCN) reaction of hydrogen [11C]cyanide with O-acetyl-L-serine followed by reduction. L-[11C]DAB was obtained with a radiochemical purity higher than 96% and with a decay corrected radiochemical
Diet, butyric acid and differentiation of gastrointestinal tract tumours.
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Butyric acid has two contrasting functional roles. As a product of fermentation within the human colon, it serves as the most important energy source for normal colorectal epithelium. It also promotes the differentiation of cultured malignant cells. A switch from aerobic to anaerobic metabolism
Two polypeptide changes associated with butyric acid resistance and the neoplastic state of Syrian hamster cells.
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Seven differences in the polypeptide species of parental Syrian hamster embryo cells and cells of the highly tumorigenic derivative cell line BP6T were identified previously by employing the technique of two-dimensional polyacrylamide gel electrophoresis (Leavitt, J. and Moyzis, R. (1978) J. Biol.
Butyric acid and tributyrin induce apoptosis in human hepatic tumour cells.
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The anti-colon cancer effect of dietary fibre results in part from its fermentation into the short-chain fatty acid butyric acid (BA) by intestinal microflora. BA has potent anti-colon cancer properties owing to its ability to induce apoptosis in colon cancer cells. The colon is not the only
Prodrugs of butyric acid. Novel derivatives possessing increased aqueous solubility and potential for treating cancer and blood diseases.
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The synthesis and biological activities of acidic, basic and neutral types of butyric acid (BA) prodrugs possessing increased aqueous solubility are described. The compounds are butyroyloxyalkyl derivatives of carboxylic acids, which possess functionalities suitable for aqueous solubilization. The
Effect of the cytostatic butyric acid pro-drug, pivaloyloxymethyl butyrate, on the tumorigenicity of cancer cells.
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Previously we have shown that pivaloyloxymethyl butyrate (AN-9), a pro-drug of butyric acid (BA), is a differentiation-inducing agent in a variety of cells. In this report, we demonstrate that AN-9 is a cytostatic but not cytotoxic agent in a myelomonocytic cell line (WEHI); thus, the cells were
An anti-cancer derivative of butyric acid (pivalyloxmethyl buterate) and daunorubicin cooperatively prolong survival of mice inoculated with monocytic leukaemia cells.
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A derivative of butyric acid, pivalyloxymethyl butyrate (AN-9), inhibited the proliferation and induced apoptosis of mouse monocytic leukaemia Mm-A cells, although sodium butyrate, but not AN-9, induced differentiation of the cells. AN-9 and DNA-specific antineoplastic agents synergistically
Stimulation of microglial metabotropic glutamate receptor mGlu2 triggers tumor necrosis factor alpha-induced neurotoxicity in concert with microglial-derived Fas ligand.
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Activated microglia may be detrimental to neuronal survival in a number of neurodegenerative diseases. Thus, strategies that reduce microglial neurotoxicity may have therapeutic benefit. Stimulation of group II metabotropic glutamate (mGlu) receptors on rat primary microglia with the specific group
Mechanism for inactivation of the KIP family cyclin-dependent kinase inhibitor genes in gastric cancer cells.
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The mechanism for inactivation of the KIP family cyclin-dependent kinase inhibitor (CDKI) genes, the p21, p27, and p57 genes, in gastric cancer cells was tested by treating the cells with either the DNA demethylation agent, 5-aza-2'-deoxycytidine or the histone deacetylase inhibitor, n-butyric acid
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