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  1. Article ; Online: Real-time resolution studies of the regulation of pyruvate-dependent lactate metabolism by hexokinases in single cells

    Scott John / Guillaume Calmettes / Shili Xu / Bernard Ribalet

    PLoS ONE, Vol 18, Iss

    2023  Volume 11

    Keywords Medicine ; R ; Science ; Q
    Language English
    Publishing date 2023-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Real-time resolution studies of the regulation of pyruvate-dependent lactate metabolism by hexokinases in single cells.

    Scott John / Guillaume Calmettes / Shili Xu / Bernard Ribalet

    PLoS ONE, Vol 18, Iss 11, p e

    2023  Volume 0286660

    Abstract: Lactate is a mitochondrial substrate for many tissues including neuron, muscle, skeletal and cardiac, as well as many cancer cells, however little is known about the processes that regulate its utilization in mitochondria. Based on the close association ... ...

    Abstract Lactate is a mitochondrial substrate for many tissues including neuron, muscle, skeletal and cardiac, as well as many cancer cells, however little is known about the processes that regulate its utilization in mitochondria. Based on the close association of Hexokinases (HK) with mitochondria, and the known cardio-protective role of HK in cardiac muscle, we have investigated the regulation of lactate and pyruvate metabolism by hexokinases (HKs), utilizing wild-type HEK293 cells and HEK293 cells in which the endogenous HKI and/or HKII have been knocked down to enable overexpression of wild type and mutant HKs. To assess the real-time changes in intracellular lactate levels the cells were transfected with a lactate specific FRET probe. In the HKI/HKII double knockdown cells, addition of extracellular pyruvate caused a large and sustained decrease in lactate. This decrease was rapidly reversed upon inhibition of the malate aspartate shuttle by aminooxyacetate, or inhibition of mitochondrial oxidative respiration by NaCN. These results suggest that in the absence of HKs, pyruvate-dependent activation of the TCA cycle together with the malate aspartate shuttle facilitates lactate transformation into pyruvate and its utilization by mitochondria. With replacement by overexpression of HKI or HKII the cellular response to pyruvate and NaCN was modified. With either hexokinase present, both the decrease in lactate due to the addition of pyruvate and the increase following addition of NaCN were either transient or suppressed altogether. Blockage of the pentose phosphate pathway with the inhibitor 6-aminonicotinamide (6-AN), abolished the effects of HK replacement. These results suggest that blocking of the malate aspartate shuttle by HK may involve activation of the pentose phosphate pathway and increased NADPH production.
    Keywords Medicine ; R ; Science ; Q
    Language English
    Publishing date 2023-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Asparagine promotes cancer cell proliferation through use as an amino acid exchange factor

    Abigail S. Krall / Shili Xu / Thomas G. Graeber / Daniel Braas / Heather R. Christofk

    Nature Communications, Vol 7, Iss 1, Pp 1-

    2016  Volume 13

    Abstract: Cancer cells have been shown to be dependent upon glutamine for growth. Here, the authors show that intracellular asparagine, a glutamine-derived metabolite, is critical to cancer cell growth and can compensate glutamine deficiency by acting as an amino ... ...

    Abstract Cancer cells have been shown to be dependent upon glutamine for growth. Here, the authors show that intracellular asparagine, a glutamine-derived metabolite, is critical to cancer cell growth and can compensate glutamine deficiency by acting as an amino acid exchange factor.
    Keywords Science ; Q
    Language English
    Publishing date 2016-04-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article: Pyrolysis Characteristics and Kinetics of Typical Municipal Solid Waste Components and Their Mixture: Analytical TG-FTIR Study

    Qiao, Yingyun / Fanfan Xu / Shili Xu / Dan Yang / Bo Wang / Xue Ming / Junhui Hao / Yuanyu Tian

    Energy & fuels. 2018 Sept. 25, v. 32, no. 10

    2018  

    Abstract: Recently, the renewed interest in the pyrolysis of municipal solid waste has been aroused. In this investigation, the pyrolysis behaviors and kinetics of typical municipal solid waste components and their mixture at high heating rates are studied by ... ...

    Abstract Recently, the renewed interest in the pyrolysis of municipal solid waste has been aroused. In this investigation, the pyrolysis behaviors and kinetics of typical municipal solid waste components and their mixture at high heating rates are studied by using thermogravimetry-Fourier transform infrared spectrometer (TG-FTIR). The TG/DTG results presented the different pyrolysis behaviors of each components and their mixture. The main volatiles were generated from 250 °C to 500 °C obtained by FTIR results. Moreover, the consistency between volatiles release and pyrolysis behavior was found through FTIR and TG. By comparing the experimental and calculated TG/DTG curves and volatiles released curves of mixed MSW, the interactions between individual components have been found, which performed as the interactions could accelerate the first pyrolysis reaction stage and postpone the second and third pyrolysis reaction stage. On the basis of the distributed activation energy model, the values of activation energy of individual components and their mixture were distributed between 123.73 kJ mol–¹ and 312.56 kJ mol–¹. Meanwhile, the frequency factor of them increased along with the activation energy. Overall, those findings can enrich a better comprehension of the MSW pyrolysis process.
    Keywords Fourier transform infrared spectroscopy ; activation energy ; differential thermal analysis ; fuels ; models ; municipal solid waste ; pyrolysis ; spectrometers ; thermogravimetry
    Language English
    Dates of publication 2018-0925
    Size p. 10801-10812.
    Publishing place American Chemical Society
    Document type Article
    ZDB-ID 1483539-3
    ISSN 1520-5029 ; 0887-0624
    ISSN (online) 1520-5029
    ISSN 0887-0624
    DOI 10.1021/acs.energyfuels.8b02571
    Database NAL-Catalogue (AGRICOLA)

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  5. Article ; Online: A precision therapeutic strategy for hexokinase 1-null, hexokinase 2-positive cancers

    Shili Xu / Arthur Catapang / Daniel Braas / Linsey Stiles / Hanna M. Doh / Jason T. Lee / Thomas G. Graeber / Robert Damoiseaux / Orian Shirihai / Harvey R. Herschman

    Cancer & Metabolism, Vol 6, Iss 1, Pp 1-

    2018  Volume 17

    Abstract: Abstract Background Precision medicine therapies require identification of unique molecular cancer characteristics. Hexokinase (HK) activity has been proposed as a therapeutic target; however, different hexokinase isoforms have not been well ... ...

    Abstract Abstract Background Precision medicine therapies require identification of unique molecular cancer characteristics. Hexokinase (HK) activity has been proposed as a therapeutic target; however, different hexokinase isoforms have not been well characterized as alternative targets. While HK2 is highly expressed in the majority of cancers, cancer subtypes with differential HK1 and HK2 expression have not been characterized for their sensitivities to HK2 silencing. Methods HK1 and HK2 expression in the Cancer Cell Line Encyclopedia dataset was analyzed. A doxycycline-inducible shRNA silencing system was used to examine the effect of HK2 knockdown in cultured cells and in xenograft models of HK1−HK2+ and HK1+HK2+ cancers. Glucose consumption and lactate production rates were measured to monitor HK activity in cell culture, and 18F-FDG PET/CT was used to monitor HK activity in xenograft tumors. A high-throughput screen was performed to search for synthetically lethal compounds in combination with HK2 inhibition in HK1−HK2+ liver cancer cells, and a combination therapy for liver cancers with this phenotype was developed. A metabolomic analysis was performed to examine changes in cellular energy levels and key metabolites in HK1−HK2+ cells treated with this combination therapy. The CRISPR Cas9 method was used to establish isogenic HK1+HK2+ and HK1−HK2+ cell lines to evaluate HK1−HK2+ cancer cell sensitivity to the combination therapy. Results Most tumors express both HK1 and HK2, and subsets of cancers from a wide variety of tissues of origin express only HK2. Unlike HK1+HK2+ cancers, HK1−HK2+ cancers are sensitive to HK2 silencing-induced cytostasis. Synthetic lethality was achieved in HK1−HK2+ liver cancer cells, by the combination of DPI, a mitochondrial complex I inhibitor, and HK2 inhibition, in HK1−HK2+ liver cancer cells. Perhexiline, a fatty acid oxidation inhibitor, further sensitizes HK1−HK2+ liver cancer cells to the complex I/HK2-targeted therapeutic combination. Although HK1+HK2+ lung cancer H460 cells are ...
    Keywords Precision medicine ; Warburg effect ; Liver cancer ; Cancer ; Glycolysis ; Hexokinase 2 ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282
    Subject code 610
    Language English
    Publishing date 2018-06-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Small Molecule Inhibitors of CXCR4

    Bikash Debnath, Shili Xu, Fedora Grande, Antonio Garofalo, Nouri Neamati

    Theranostics, Vol 3, Iss 1, Pp 47-

    2013  Volume 75

    Abstract: CXCR4 is a G-protein-coupled receptor involved in a number of physiological processes in the hematopoietic and immune systems. The SDF-1/CXCR4 axis is significantly associated with several diseases, such as HIV, cancer, WHIM syndrome, rheumatoid ... ...

    Abstract CXCR4 is a G-protein-coupled receptor involved in a number of physiological processes in the hematopoietic and immune systems. The SDF-1/CXCR4 axis is significantly associated with several diseases, such as HIV, cancer, WHIM syndrome, rheumatoid arthritis, pulmonary fibrosis and lupus. For example, CXCR4 is one of the major co-receptors for HIV entry into target cells, while in cancer it plays an important role in tumor cell metastasis. Several promising CXCR4 antagonists have been developed to block SDF-1/CXCR4 interactions that are currently under different stages of development. The first in class CXCR4 antagonist, plerixafor, was approved by the FDA in 2008 for the mobilization of hematopoietic stem cells and several other drugs are currently in clinical trials for cancer, HIV, and WHIM syndrome. While the long-term safety data for the first generation CXCR4 antagonists are not yet available, several new compounds are under preclinical development in an attempt to provide safer and more efficient treatment options for HIV and cancer patients.
    Keywords Medicine ; R
    Subject code 610
    Language English
    Publishing date 2013-01-01T00:00:00Z
    Publisher Ivyspring International Publisher
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Chronic IL-1β-induced inflammation regulates epithelial-to-mesenchymal transition memory phenotypes via epigenetic modifications in non-small cell lung cancer

    Rui Li / Stephanie L. Ong / Linh M. Tran / Zhe Jing / Bin Liu / Stacy J. Park / Zi Ling Huang / Tonya C. Walser / Eileen L. Heinrich / Gina Lee / Ramin Salehi-Rad / William P. Crosson / Paul C. Pagano / Manash K. Paul / Shili Xu / Harvey Herschman / Kostyantyn Krysan / Steven Dubinett

    Scientific Reports, Vol 10, Iss 1, Pp 1-

    2020  Volume 15

    Abstract: Abstract Chronic inflammation facilitates tumor progression. We discovered that a subset of non-small cell lung cancer cells underwent a gradually progressing epithelial-to-mesenchymal (EMT) phenotype following a 21-day exposure to IL-1β, an abundant ... ...

    Abstract Abstract Chronic inflammation facilitates tumor progression. We discovered that a subset of non-small cell lung cancer cells underwent a gradually progressing epithelial-to-mesenchymal (EMT) phenotype following a 21-day exposure to IL-1β, an abundant proinflammatory cytokine in the at-risk for lung cancer pulmonary and the lung tumor microenvironments. Pathway analysis of the gene expression profile and in vitro functional studies revealed that the EMT and EMT-associated phenotypes, including enhanced cell invasion, PD-L1 upregulation, and chemoresistance, were sustained in the absence of continuous IL-1β exposure. We referred to this phenomenon as EMT memory. Utilizing a doxycycline-controlled SLUG expression system, we found that high expression of the transcription factor SLUG was indispensable for the establishment of EMT memory. High SLUG expression in tumors of lung cancer patients was associated with poor survival. Chemical or genetic inhibition of SLUG upregulation prevented EMT following the acute IL-1β exposure but did not reverse EMT memory. Chromatin immunoprecipitation and methylation-specific PCR further revealed a SLUG-mediated temporal regulation of epigenetic modifications, including accumulation of H3K27, H3K9, and DNA methylation, in the CDH1 (E-cadherin) promoter following the chronic IL-1β exposure. Chemical inhibition of DNA methylation not only restored E-cadherin expression in EMT memory, but also primed cells for chemotherapy-induced apoptosis.
    Keywords Medicine ; R ; Science ; Q
    Subject code 610 ; 570
    Language English
    Publishing date 2020-01-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Development and Application of FASA, a Model for Quantifying Fatty Acid Metabolism Using Stable Isotope Labeling

    Joseph P. Argus / Moses Q. Wilks / Quan D. Zhou / Wei Yuan Hsieh / Elvira Khialeeva / Xen Ping Hoi / Viet Bui / Shili Xu / Amy K. Yu / Eric S. Wang / Harvey R. Herschman / Kevin J. Williams / Steven J. Bensinger

    Cell Reports, Vol 25, Iss 10, Pp 2919-2934.e

    2018  Volume 8

    Abstract: Summary: It is well understood that fatty acids can be synthesized, imported, and modified to meet requisite demands in cells. However, following the movement of fatty acids through the multiplicity of these metabolic steps has remained difficult. To ... ...

    Abstract Summary: It is well understood that fatty acids can be synthesized, imported, and modified to meet requisite demands in cells. However, following the movement of fatty acids through the multiplicity of these metabolic steps has remained difficult. To better address this problem, we developed Fatty Acid Source Analysis (FASA), a model that defines the contribution of synthesis, import, and elongation pathways to fatty acid homeostasis in saturated, monounsaturated, and polyunsaturated fatty acid pools. Application of FASA demonstrated that elongation can be a major contributor to cellular fatty acid content and showed that distinct pro-inflammatory stimuli (e.g., Toll-like receptors 2, 3, or 4) specifically reprogram homeostasis of fatty acids by differential utilization of synthetic and elongation pathways in macrophages. In sum, this modeling approach significantly advances our ability to interrogate cellular fatty acid metabolism and provides insight into how cells dynamically reshape their lipidomes in response to metabolic or inflammatory signals. : Argus et al. developed Fatty Acid Source Analysis (FASA), a model that quantifies cellular fatty acid synthesis, elongation, and import. FASA is used to demonstrate that elongation can be a major contributor to cellular fatty acid content and that different stimuli reprogram macrophage fatty acid elongation pathways in distinct ways. Keywords: fatty acid homeostasis, fatty acid modeling, stable isotope labeling
    Keywords Biology (General) ; QH301-705.5
    Subject code 571
    Language English
    Publishing date 2018-12-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Loss of survivin in the prostate epithelium impedes carcinogenesis in a mouse model of prostate adenocarcinoma.

    Helty Adisetiyo / Mengmeng Liang / Chun-Peng Liao / Ari Aycock-Williams / Michael B Cohen / Shili Xu / Nouri Neamati / Edward M Conway / Chieh-Yang Cheng / Alexander Yu Nikitin / Pradip Roy-Burman

    PLoS ONE, Vol 8, Iss 7, p e

    2013  Volume 69484

    Abstract: The inhibitor of apoptosis protein survivin is expressed in most cancers. Using the conditional PTEN deletion mouse model, we previously reported that survivin levels increase with prostate tumor growth. Here we evaluated the functional role of survivin ... ...

    Abstract The inhibitor of apoptosis protein survivin is expressed in most cancers. Using the conditional PTEN deletion mouse model, we previously reported that survivin levels increase with prostate tumor growth. Here we evaluated the functional role of survivin in prostate tumor growth. First, we demonstrated that mice lacking the survivin gene in prostate epithelium were fertile and had normal prostate growth and development. We then serially, from about 10-56 weeks of age, evaluated histopathologic changes in the prostate of mice with PTEN deletion combined with survivin mono- or bi-allelic gene deletion. While within this time period most of the animals with wild-type or monoallelic survivin deletion developed adenocarcinomas, the most severe lesions in the biallelic survivin deleted mice were high-grade prostatic intra-epithelial neoplasia with distinct histopathology. Many atypical cells contained large hypertrophic cytoplasm and desmoplastic reaction in the prostatic intra-epithelial neoplasia lesions of this group was minimal until the late ages. A reduced proliferation index as well as apoptotic and senescent cells were detected in the lesions of mice with compound PTEN/survivin deficiency throughout the time points examined. Survivin deletion was also associated with reduced tumor expression of another inhibitor of apoptosis member, the X-linked inhibitor of apoptosis. Our findings suggest that survivin participates in the progression of prostatic intraepithelial neoplasia to adenocarcinoma, and that survivin interference at the prostatic intraepithelial neoplasia stages may be a potential therapeutic strategy to halt or delay further progression.
    Keywords Medicine ; R ; Science ; Q
    Subject code 570
    Language English
    Publishing date 2013-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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