udp glucose/breast neoplasms

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Inhibition of human UDP-glucose dehydrogenase expression using siRNA expression vector in breast cancer cells.

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UDP-glucose dehydrogenase (UGDH) catalyzes two oxidations of UDP-glucose to yield UDP-glucuronic acid. Pathological over-production of extracellular matrix components may be linked to the availability of UDP-glucuronic acid, therefore UGDH is a potential therapeutic target. RNA interference (RNAi)

UDP-glucose 6-dehydrogenase knockout impairs migration and decreases in vivo metastatic ability of breast cancer cells

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Dysregulated metabolism is a hallmark of cancer that supports tumor growth and metastasis. One understudied aspect of cancer metabolism is altered nucleotide sugar biosynthesis, which drives aberrant cell surface glycosylation known to support various aspects of cancer cell behavior including

UDP-glucose ceramide glucosyltransferase activates AKT, promoted proliferation, and doxorubicin resistance in breast cancer cells.

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The UDP-glucose ceramide glucosyltransferase (UGCG) is a key enzyme in the synthesis of glycosylated sphingolipids, since this enzyme generates the precursor for all complex glycosphingolipids (GSL), the GlcCer. The UGCG has been associated with several cancer-related processes such as maintaining

UDP-glucose 6-dehydrogenase regulates hyaluronic acid production and promotes breast cancer progression.

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An improved understanding of the biochemical alterations that accompany tumor progression and metastasis is necessary to inform the next generation of diagnostic tools and targeted therapies. Metabolic reprogramming is known to occur during the epithelial-mesenchymal transition (EMT), a process that

Correction: UDP-glucose 6-dehydrogenase regulates hyaluronic acid production and promotes breast cancer progression.

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An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Inhibitory effects of gallic acid and quercetin on UDP-glucose dehydrogenase activity.

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We have examined polyphenols as potential inhibitors of UDP-glucose dehydrogenase (UGDH) activity. Gallic acid and quercetin decreased specific activities of UGDH and inhibited the proliferation of MCF-7 human breast cancer cells. Western blot analysis showed that gallic acid and quercetin did not

Hormone dependence of breast cancer cells and the effects of tamoxifen and estrogen: 31P NMR studies.

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Many breast tumors appear to progress from estrogen-dependent growth to a more malignant phenotype characterized by estrogen-independent growth, antiestrogen resistance, and a high metastatic potential. Utilizing 31P NMR spectroscopy on human breast cancer cells growing in vitro, we have

Identification and cloning of a novel androgen-responsive gene, uridine diphosphoglucose dehydrogenase, in human breast cancer cells.

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Androgens inhibit the growth of breast cancer cells, but the mechanism of androgen-induced growth inhibition has not yet been elucidated, and few androgen-responsive genes have been identified. We, therefore, used differential display PCR to identify novel androgen-responsive genes in ZR-75-1 human

MDR1 (multidrug resistence 1) can regulate GCS (glucosylceramide synthase) in breast cancer cells.

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OBJECTIVE Besides MDR1/P-glycoprotein (MDR1/P-gp), glucosylceramide synthase (GCS), an enzyme, which transfers UDP-glucose to ceramide to form glucosylceramide was also related with multidrug resistance (MDR) in breast cancer. Although many research showed that GCS could affect mdr1 in cancer cells,

UGCG influences glutamine metabolism of breast cancer cells.

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UDP-glucose ceramide glucosyltransferase (UGCG) is the key enzyme in glycosphingolipid (GSL) metabolism by being the only enzyme that generates glucosylceramide (GlcCer) de novo. Increased UGCG synthesis is associated with pro-cancerous processes such as increased proliferation and multidrug

Increased ceramide production sensitizes breast cancer cell response to chemotherapy.

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BACKGROUND Advanced breast cancer remains clinically challenging due to its resistance to chemotherapy. To understand the underlying mechanisms of resistance and identify drugable target, the involvement of ceramide metabolism is investigated. METHODS Ceramide levels in breast cancer tissues derived

UGCG Overexpression Leads to Increased Glycolysis and Increased Oxidative Phosphorylation of Breast Cancer Cells

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The only enzyme in the glycosphingolipid (GSL) metabolic pathway, which produces glucosylceramide (GlcCer) de novo is UDP-glucose ceramide glucosyltransferase (UGCG). UGCG is linked to pro-cancerous processes such as multidrug resistance development and increased proliferation in several cancer

Acute leukemia cells resistant to PI3K/mTOR inhibition display upregulation of P2RY14 expression.

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The PI3K/mTOR pathway is the second most frequently deregulated pathway in a majority of cancers such as breast cancer, lung cancer, and melanomas as well as leukemia. Mutations in the genes coding for receptor tyrosine kinases (RTKs) and G-protein-coupled receptors (GPCRs) are quite common in all

Glucosylation of the peptide leucinostatin A, produced by an endophytic fungus of European yew, may protect the host from leucinostatin toxicity.

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BACKGROUND Yew species (Taxus spp.) throughout the world are hosts to hundreds, or perhaps thousands, of endophytic organisms. Most commonly, these organisms are fungi, living in a commensal or a symbiotic relationship with their host plant, so the plants exhibit little or no outward evidence that

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