Publications (26) View all
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Article: Dysregulation of glucose transport, glycolysis, TCA cycle and glutaminolysis by oncogenes and tumor suppressors in cancer cells.
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ABSTRACT: A common set of functional characteristics of cancer cells is that cancer cells consume a large amount of glucose, maintain high rate of glycolysis and convert a majority of glucose into lactic acid even in the presence of oxygen compared to that of normal cells (Warburg's Effects). In addition, cancer cells exhibit substantial alterations in several energy metabolism pathways including glucose transport, tricarboxylic acid (TCA) cycle, glutaminolysis, mitochondrial respiratory chain oxidative phosphorylation and pentose phosphate pathway (PPP). In the present work, we focused on reviewing the current knowledge about the dysregulation of the proteins/enzymes involved in the key regulatory steps of glucose transport, glycolysis, TCA cycle and glutaminolysis by several oncogenes including c-Myc and hypoxia inducible factor-1 (HIF-1) and tumor suppressor, p53, in cancer cells. The dysregulation of glucose transport and energy metabolism pathways by oncogenes and lost functions of the tumor suppressors have been implicated as important biomarkers for cancer detection and as valuable targets for the development of new anticancer therapies.Biochimica et Biophysica Acta 06/2012; 1826(12):370-84. · 4.66 Impact Factor -
Article: Real-time PCR methodology for selective detection of viable Escherichia coli O157:H7 cells by targeting Z3276 as a genetic marker.
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ABSTRACT: The goal of this study was to develop a sensitive, specific, and accurate method for the selective detection of viable Escherichia coli O157:H7 cells in foods. A unique open reading frame (ORF), Z3276, was identified as a specific genetic marker for the detection of E. coli O157:H7. We developed a real-time PCR assay with primers and probe targeting ORF Z3276 and confirmed that this assay was sensitive and specific for E. coli O157:H7 strains (n = 298). Using this assay, we can detect amounts of genomic DNA of E. coli O157:H7 as low as a few CFU equivalents. Moreover, we have developed a new propidium monoazide (PMA)-real-time PCR protocol that allows for the clear differentiation of viable from dead cells. In addition, the protocol was adapted to a 96-well plate format for easy and consistent handling of a large number of samples. Amplification of DNA from PMA-treated dead cells was almost completely inhibited, in contrast to the virtually unaffected amplification of DNA from PMA-treated viable cells. With beef spiked simultaneously with 8 × 10(7) dead cells/g and 80 CFU viable cells/g, we were able to selectively detect viable E. coli O157:H7 cells with an 8-h enrichment. In conclusion, this PMA-real-time PCR assay offers a sensitive and specific means to selectively detect viable E. coli O157:H7 cells in spiked beef. It also has the potential for high-throughput selective detection of viable E. coli O157:H7 cells in other food matrices and, thus, will have an impact on the accurate microbiological and epidemiological monitoring of food safety and environmental sources.Applied and environmental microbiology 05/2012; 78(15):5297-304. · 3.69 Impact Factor -
Article: Mitochondrial oestrogen receptors and their potential implications in oestrogen carcinogenesis in human breast cancer
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ABSTRACT: Background. Prolonged exposure to oestrogens (17β‐estradiol)(E2), xenoestrogens, hormone replacement therapy and contraceptives has been recognized as a key aetiological factor of human breast cancer. The biological and carcinogenic effects of E2 and xenoestrogens are mediated via oestrogen receptors alpha (ERα) and beta (ERβ). Both receptors are localized in the nucleus of E2‐targeted cells including human breast cells where they are involved in the regulation of nuclear gene expression. There is increasing evidence indicating that a small fraction of total cellular ERs, particularly ERα, are localized in the membrane of E2‐targeted cells where they mediate E2‐dependent and/or E2‐independent rapid and non‐nuclear genomic signal pathways. Results. The present work will present evidence that: (1) there is mitochondrial localization of ERs in human breast cancer cells; (2) there is a functional role of the mitochondrial ERs in the regulation of mitochondrial genes encoding respiratory chain proteins. Conclusions. The potential implications of the mitochondrial ER‐mediated pathways in oestrogen carcinogenesis, particularly in stimulation of cell proliferation and inhibition of apoptosis, in human breast cancer and the potential nutritional and environmental perspectives of these effects will be addressed.07/2009; 17(1):76-89. -
Article: Mechanisms of hormone carcinogenesis: evolution of views, role of mitochondria.
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ABSTRACT: CumuIative and excessive exposure to estrogens is associated with increased breast cancer risk. The traditional mechanism explaining this association is that estrogens affect the rate of cell division and apoptosis and thus manifest their effect on the risk of breast cancer by affecting the growth of breast epithelial tissues. Highly proliferative cells are susceptible to genetic errors during DNA replication. The action of estrogen metabolites offers a complementary genotoxic pathway mediated by the generation of reactive estrogen quinone metabolites that can form adducts with DNA and generate reactive oxygen species through redox cycling. In this chapter, we discussed a novel mitochondrial pathway mediated by estrogens and their cognate estrogen receptors (ERs) and its potential implications in estrogen-dependent carcinogenesis. Several lines of evidence are presented to show: (1) mitochondrial localization of ERs in human breast cancer cells and other cell types; (2) a functional role for the mitochondrial ERs in regulation of the mitochondrial respiratory chain (MRC) proteins and (3) potential implications of the mitochondrial ER-mediated pathway in stimulation of cell proliferation, inhibition of apoptosis and oxidative damage to mitochondrial DNA. The possible involvement of estrogens and ERs in deregulation of mitochondrial bioenergetics, an important hallmark of cancer cells, is also described. An evolutionary view is presented to suggest that persistent stimulation by estrogens through ER signaling pathways of MRC proteins and energy metabolic pathways leads to the alterations in mitochondrial bioenergetics and contributes to the development of estrogen-related cancers.Advances in experimental medicine and biology 01/2008; 630:1-18. · 1.09 Impact Factor -
Article: Chen, JQ*, Eshete, M, Alworth, WL, and Yager, JD (2004) Binding of MCF-7 cell mitochondrial proteins and recombinant human estrogen receptors alpha and beta to human mitochondrial DNA estrogen response elements. J Cell Biochem 93:358-373.
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