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  1. Article ; Online: Loss of attachment promotes proline accumulation and excretion in cancer cells.

    Pilley, Steven E / Hennequart, Marc / Vandekeere, Anke / Blagih, Julianna / Legrave, Nathalie M / Fendt, Sarah-Maria / Vousden, Karen H / Labuschagne, Christiaan F

    Science advances

    2023  Volume 9, Issue 36, Page(s) eadh2023

    Abstract: Previous studies have revealed a role for proline metabolism in supporting cancer development and metastasis. In this study, we show that many cancer cells respond to loss of attachment by accumulating and secreting proline. Detached cells display ... ...

    Abstract Previous studies have revealed a role for proline metabolism in supporting cancer development and metastasis. In this study, we show that many cancer cells respond to loss of attachment by accumulating and secreting proline. Detached cells display reduced proliferation accompanied by a general decrease in overall protein production and de novo amino acid synthesis compared to attached cells. However, proline synthesis was maintained under detached conditions. Furthermore, while overall proline incorporation into proteins was lower in detached cells compared to other amino acids, there was an increased production of the proline-rich protein collagen. The increased excretion of proline from detached cells was also shown to be used by macrophages, an abundant and important component of the tumor microenvironment. Our study suggests that detachment induced accumulation and secretion of proline may contribute to tumor progression by supporting increased production of extracellular matrix and providing proline to surrounding stromal cells.
    MeSH term(s) Proline ; Amino Acids ; Biological Transport ; Extracellular Matrix ; Macrophages ; Neoplasms
    Chemical Substances Proline (9DLQ4CIU6V) ; Amino Acids
    Language English
    Publishing date 2023-09-06
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.adh2023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Phenotypic profiling of solute carriers characterizes serine transport in cancer.

    Papalazarou, Vasileios / Newman, Alice C / Huerta-Uribe, Alejandro / Legrave, Nathalie M / Falcone, Mattia / Zhang, Tong / McGarry, Lynn / Athineos, Dimitris / Shanks, Emma / Blyth, Karen / Vousden, Karen H / Maddocks, Oliver D K

    Nature metabolism

    2023  Volume 5, Issue 12, Page(s) 2148–2168

    Abstract: Serine is a vital amino acid in tumorigenesis. While cells can perform de novo serine synthesis, most transformed cells rely on serine uptake to meet their increased biosynthetic requirements. Solute carriers (SLCs), a family of transmembrane nutrient ... ...

    Abstract Serine is a vital amino acid in tumorigenesis. While cells can perform de novo serine synthesis, most transformed cells rely on serine uptake to meet their increased biosynthetic requirements. Solute carriers (SLCs), a family of transmembrane nutrient transport proteins, are the gatekeepers of amino acid acquisition and exchange in mammalian cells and are emerging as anticancer therapeutic targets; however, the SLCs that mediate serine transport in cancer cells remain unknown. Here we perform an arrayed RNAi screen of SLC-encoding genes while monitoring amino acid consumption and cell proliferation in colorectal cancer cells using metabolomics and high-throughput imaging. We identify SLC6A14 and SLC25A15 as major cytoplasmic and mitochondrial serine transporters, respectively. We also observe that SLC12A4 facilitates serine uptake. Dual targeting of SLC6A14 and either SLC25A15 or SLC12A4 diminishes serine uptake and growth of colorectal cancer cells in vitro and in vivo, particularly in cells with compromised de novo serine biosynthesis. Our results provide insight into the mechanisms that contribute to serine uptake and intracellular handling.
    MeSH term(s) Animals ; Membrane Transport Proteins/metabolism ; Biological Transport ; Amino Acids/metabolism ; Serine/metabolism ; Colorectal Neoplasms/genetics ; Mammals/metabolism
    Chemical Substances Membrane Transport Proteins ; Amino Acids ; Serine (452VLY9402)
    Language English
    Publishing date 2023-12-08
    Publishing country Germany
    Document type Journal Article
    ISSN 2522-5812
    ISSN (online) 2522-5812
    DOI 10.1038/s42255-023-00936-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The impact of physiological metabolite levels on serine uptake, synthesis and utilization in cancer cells.

    Hennequart, Marc / Labuschagne, Christiaan F / Tajan, Mylène / Pilley, Steven E / Cheung, Eric C / Legrave, Nathalie M / Driscoll, Paul C / Vousden, Karen H

    Nature communications

    2021  Volume 12, Issue 1, Page(s) 6176

    Abstract: Serine is a non-essential amino acid that is critical for tumour proliferation and depletion of circulating serine results in reduced tumour growth and increased survival in various cancer models. While many cancer cells cultured in a standard tissue ... ...

    Abstract Serine is a non-essential amino acid that is critical for tumour proliferation and depletion of circulating serine results in reduced tumour growth and increased survival in various cancer models. While many cancer cells cultured in a standard tissue culture medium depend on exogenous serine for optimal growth, here we report that these cells are less sensitive to serine/glycine depletion in medium containing physiological levels of metabolites. The lower requirement for exogenous serine under these culture conditions reflects both increased de novo serine synthesis and the use of hypoxanthine (not present in the standard medium) to support purine synthesis. Limiting serine availability leads to increased uptake of extracellular hypoxanthine, sparing available serine for other pathways such as glutathione synthesis. Taken together these results improve our understanding of serine metabolism in physiologically relevant nutrient conditions and allow us to predict interventions that may enhance the therapeutic response to dietary serine/glycine limitation.
    MeSH term(s) Biosynthetic Pathways ; Cell Line, Tumor ; Cell Proliferation ; Culture Media/chemistry ; Culture Media/metabolism ; Glycine/analysis ; Glycine/metabolism ; Humans ; Hypoxanthine/analysis ; Hypoxanthine/metabolism ; Neoplasms/diet therapy ; Neoplasms/metabolism ; Neoplasms/pathology ; Purines/biosynthesis ; Serine/analysis ; Serine/metabolism ; Up-Regulation
    Chemical Substances Culture Media ; Purines ; Hypoxanthine (2TN51YD919) ; Serine (452VLY9402) ; Glycine (TE7660XO1C)
    Language English
    Publishing date 2021-10-26
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-021-26395-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: The dietary sweetener sucralose is a negative modulator of T cell-mediated responses.

    Zani, Fabio / Blagih, Julianna / Gruber, Tim / Buck, Michael D / Jones, Nicholas / Hennequart, Marc / Newell, Clare L / Pilley, Steven E / Soro-Barrio, Pablo / Kelly, Gavin / Legrave, Nathalie M / Cheung, Eric C / Gilmore, Ian S / Gould, Alex P / Garcia-Caceres, Cristina / Vousden, Karen H

    Nature

    2023  Volume 615, Issue 7953, Page(s) 705–711

    Abstract: Artificial sweeteners are used as calorie-free sugar substitutes in many food products and their consumption has increased substantially over the past ... ...

    Abstract Artificial sweeteners are used as calorie-free sugar substitutes in many food products and their consumption has increased substantially over the past years
    MeSH term(s) Animals ; Mice ; Sucrose/analogs & derivatives ; Sweetening Agents/administration & dosage ; Sweetening Agents/adverse effects ; Sweetening Agents/pharmacology ; Sweetening Agents/therapeutic use ; T-Lymphocytes/drug effects ; T-Lymphocytes/immunology ; T-Lymphocytes/pathology ; Food Safety ; Calcium Signaling/drug effects ; Receptors, Antigen, T-Cell/drug effects ; Receptors, Antigen, T-Cell/immunology ; Bacterial Infections/immunology ; Neoplasms/immunology ; Autoimmunity/drug effects ; Autoimmunity/immunology ; CD8-Positive T-Lymphocytes/drug effects ; CD8-Positive T-Lymphocytes/immunology
    Chemical Substances Sucrose (57-50-1) ; Sweetening Agents ; trichlorosucrose (96K6UQ3ZD4) ; Receptors, Antigen, T-Cell
    Language English
    Publishing date 2023-03-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/s41586-023-05801-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: ALDH1L2 regulation of formate, formyl-methionine, and ROS controls cancer cell migration and metastasis.

    Hennequart, Marc / Pilley, Steven E / Labuschagne, Christiaan F / Coomes, Jack / Mervant, Loic / Driscoll, Paul C / Legrave, Nathalie M / Lee, Younghwan / Kreuzaler, Peter / Macintyre, Benedict / Panina, Yulia / Blagih, Julianna / Stevenson, David / Strathdee, Douglas / Schneider-Luftman, Deborah / Grönroos, Eva / Cheung, Eric C / Yuneva, Mariia / Swanton, Charles /
    Vousden, Karen H

    Cell reports

    2023  Volume 42, Issue 6, Page(s) 112562

    Abstract: Mitochondrial 10-formyltetrahydrofolate (10-formyl-THF) is utilized by three mitochondrial enzymes to produce formate for nucleotide synthesis, NADPH for antioxidant defense, and formyl-methionine (fMet) to initiate mitochondrial mRNA translation. One of ...

    Abstract Mitochondrial 10-formyltetrahydrofolate (10-formyl-THF) is utilized by three mitochondrial enzymes to produce formate for nucleotide synthesis, NADPH for antioxidant defense, and formyl-methionine (fMet) to initiate mitochondrial mRNA translation. One of these enzymes-aldehyde dehydrogenase 1 family member 2 (ALDH1L2)-produces NADPH by catabolizing 10-formyl-THF into CO
    MeSH term(s) Female ; Humans ; Breast Neoplasms/metabolism ; Formates/metabolism ; Methionine ; NADP ; Reactive Oxygen Species ; Oxidoreductases Acting on CH-NH Group Donors/metabolism
    Chemical Substances Formates ; Methionine (AE28F7PNPL) ; NADP (53-59-8) ; Reactive Oxygen Species ; 10-formyltetrahydropteroylglutamic acid (2800-34-2) ; formyltetrahydrofolate dehydrogenase (EC 1.5.1.6) ; Oxidoreductases Acting on CH-NH Group Donors (EC 1.5.-)
    Language English
    Publishing date 2023-05-26
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2023.112562
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Protein Kinase C-β Dictates B Cell Fate by Regulating Mitochondrial Remodeling, Metabolic Reprogramming, and Heme Biosynthesis.

    Tsui, Carlson / Martinez-Martin, Nuria / Gaya, Mauro / Maldonado, Paula / Llorian, Miriam / Legrave, Nathalie M / Rossi, Merja / MacRae, James I / Cameron, Angus J / Parker, Peter J / Leitges, Michael / Bruckbauer, Andreas / Batista, Facundo D

    Immunity

    2018  Volume 48, Issue 6, Page(s) 1144–1159.e5

    Abstract: PKCβ-null ( ... ...

    Abstract PKCβ-null (Prkcb
    MeSH term(s) Animals ; B-Lymphocytes/immunology ; Cell Differentiation/immunology ; Heme/biosynthesis ; Lymphocyte Activation/immunology ; Mice ; Mice, Knockout ; Mitochondria/immunology ; Mitochondria/metabolism ; Plasma Cells/cytology ; Plasma Cells/immunology ; Protein Kinase C beta/immunology
    Chemical Substances Heme (42VZT0U6YR) ; Protein Kinase C beta (EC 2.7.11.13)
    Language English
    Publishing date 2018-06-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2018.04.031
    Database MEDical Literature Analysis and Retrieval System OnLINE

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