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  1. Article ; Online: Supply and demand: Cellular nutrient uptake and exchange in cancer.

    Papalazarou, Vasileios / Maddocks, Oliver D K

    Molecular cell

    2021  Volume 81, Issue 18, Page(s) 3731–3748

    Abstract: Nutrient supply and demand delineate cell behavior in health and disease. Mammalian cells have developed multiple strategies to secure the necessary nutrients that fuel their metabolic needs. This is more evident upon disruption of homeostasis in ... ...

    Abstract Nutrient supply and demand delineate cell behavior in health and disease. Mammalian cells have developed multiple strategies to secure the necessary nutrients that fuel their metabolic needs. This is more evident upon disruption of homeostasis in conditions such as cancer, when cells display high proliferation rates in energetically challenging conditions where nutritional sources may be scarce. Here, we summarize the main routes of nutrient acquisition that fuel mammalian cells and their implications in tumorigenesis. We argue that the molecular mechanisms of nutrient acquisition not only tip the balance between nutrient supply and demand but also determine cell behavior upon nutrient limitation and energetic stress and contribute to nutrient partitioning and metabolic coordination between different cell types in inflamed or tumorigenic environments.
    MeSH term(s) ATP-Binding Cassette Transporters/metabolism ; Animals ; Biological Transport/physiology ; Carcinogenesis/metabolism ; Cell Membrane/metabolism ; Homeostasis/physiology ; Humans ; Membrane Transport Proteins/metabolism ; Neoplasms/metabolism ; Nutrients/metabolism ; Solute Carrier Proteins/metabolism
    Chemical Substances ATP-Binding Cassette Transporters ; Membrane Transport Proteins ; Solute Carrier Proteins
    Language English
    Publishing date 2021-09-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1415236-8
    ISSN 1097-4164 ; 1097-2765
    ISSN (online) 1097-4164
    ISSN 1097-2765
    DOI 10.1016/j.molcel.2021.08.026
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: SERIneALanine Killer: SPT promiscuity inhibits tumour growth via intra-tumoral deoxysphingolipid production.

    Falcone, Mattia / Maddocks, Oliver D K

    Signal transduction and targeted therapy

    2020  Volume 5, Issue 1, Page(s) 274

    MeSH term(s) Humans ; Neoplasms/drug therapy ; Serine ; Sphingolipids
    Chemical Substances Sphingolipids ; Serine (452VLY9402)
    Language English
    Publishing date 2020-11-24
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2886872-9
    ISSN 2059-3635 ; 2095-9907
    ISSN (online) 2059-3635
    ISSN 2095-9907
    DOI 10.1038/s41392-020-00401-6
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  3. Article ; Online: The KRAS-BCAA-BCAT2 axis in PDAC development.

    Falcone, Mattia / Maddocks, Oliver D K

    Nature cell biology

    2020  Volume 22, Issue 2, Page(s) 139–140

    MeSH term(s) Carcinoma, Pancreatic Ductal ; Humans ; Minor Histocompatibility Antigens ; Pancreatic Neoplasms ; Pregnancy Proteins ; Proto-Oncogene Proteins p21(ras) ; Transaminases
    Chemical Substances KRAS protein, human ; Minor Histocompatibility Antigens ; Pregnancy Proteins ; Transaminases (EC 2.6.1.-) ; BCAT2 protein, human (EC 2.6.1.42) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
    Language English
    Publishing date 2020-02-05
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 1474722-4
    ISSN 1476-4679 ; 1465-7392
    ISSN (online) 1476-4679
    ISSN 1465-7392
    DOI 10.1038/s41556-020-0467-2
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  4. Article ; Online: SERIneALanine Killer

    Mattia Falcone / Oliver D. K. Maddocks

    Signal Transduction and Targeted Therapy, Vol 5, Iss 1, Pp 1-

    SPT promiscuity inhibits tumour growth via intra-tumoral deoxysphingolipid production

    2020  Volume 2

    Keywords Medicine ; R ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2020-11-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article: Supply and demand: Cellular nutrient uptake and exchange in cancer

    Papalazarou, Vasileios / Maddocks, Oliver D.K.

    Molecular cell. 2021 Sept. 16, v. 81, no. 18

    2021  

    Abstract: Nutrient supply and demand delineate cell behavior in health and disease. Mammalian cells have developed multiple strategies to secure the necessary nutrients that fuel their metabolic needs. This is more evident upon disruption of homeostasis in ... ...

    Abstract Nutrient supply and demand delineate cell behavior in health and disease. Mammalian cells have developed multiple strategies to secure the necessary nutrients that fuel their metabolic needs. This is more evident upon disruption of homeostasis in conditions such as cancer, when cells display high proliferation rates in energetically challenging conditions where nutritional sources may be scarce. Here, we summarize the main routes of nutrient acquisition that fuel mammalian cells and their implications in tumorigenesis. We argue that the molecular mechanisms of nutrient acquisition not only tip the balance between nutrient supply and demand but also determine cell behavior upon nutrient limitation and energetic stress and contribute to nutrient partitioning and metabolic coordination between different cell types in inflamed or tumorigenic environments.
    Keywords carcinogenesis ; homeostasis ; mammals ; nutrient uptake ; supply balance
    Language English
    Dates of publication 2021-0916
    Size p. 3731-3748.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 1415236-8
    ISSN 1097-4164 ; 1097-2765
    ISSN (online) 1097-4164
    ISSN 1097-2765
    DOI 10.1016/j.molcel.2021.08.026
    Database NAL-Catalogue (AGRICOLA)

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  6. 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
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  7. Article: Global metabolic alterations in colorectal cancer cells during irinotecan-induced DNA replication stress.

    Marx, Christian / Sonnemann, Jürgen / Maddocks, Oliver D K / Marx-Blümel, Lisa / Beyer, Mandy / Hoelzer, Doerte / Thierbach, René / Maletzki, Claudia / Linnebacher, Michael / Heinzel, Thorsten / Krämer, Oliver H

    Cancer & metabolism

    2022  Volume 10, Issue 1, Page(s) 10

    Abstract: Background: Metabolic adaptations can allow cancer cells to survive DNA-damaging chemotherapy. This unmet clinical challenge is a potential vulnerability of cancer. Accordingly, there is an intense search for mechanisms that modulate cell metabolism ... ...

    Abstract Background: Metabolic adaptations can allow cancer cells to survive DNA-damaging chemotherapy. This unmet clinical challenge is a potential vulnerability of cancer. Accordingly, there is an intense search for mechanisms that modulate cell metabolism during anti-tumor therapy. We set out to define how colorectal cancer CRC cells alter their metabolism upon DNA replication stress and whether this provides opportunities to eliminate such cells more efficiently.
    Methods: We incubated p53-positive and p53-negative permanent CRC cells and short-term cultured primary CRC cells with the topoisomerase-1 inhibitor irinotecan and other drugs that cause DNA replication stress and consequently DNA damage. We analyzed pro-apoptotic mitochondrial membrane depolarization and cell death with flow cytometry. We evaluated cellular metabolism with immunoblotting of electron transport chain (ETC) complex subunits, analysis of mitochondrial mRNA expression by qPCR, MTT assay, measurements of oxygen consumption and reactive oxygen species (ROS), and metabolic flux analysis with the Seahorse platform. Global metabolic alterations were assessed using targeted mass spectrometric analysis of extra- and intracellular metabolites.
    Results: Chemotherapeutics that cause DNA replication stress induce metabolic changes in p53-positive and p53-negative CRC cells. Irinotecan enhances glycolysis, oxygen consumption, mitochondrial ETC activation, and ROS production in CRC cells. This is connected to increased levels of electron transport chain complexes involving mitochondrial translation. Mass spectrometric analysis reveals global metabolic adaptations of CRC cells to irinotecan, including the glycolysis, tricarboxylic acid cycle, and pentose phosphate pathways. P53-proficient CRC cells, however, have a more active metabolism upon DNA replication stress than their p53-deficient counterparts. This metabolic switch is a vulnerability of p53-positive cells to irinotecan-induced apoptosis under glucose-restricted conditions.
    Conclusion: Drugs that cause DNA replication stress increase the metabolism of CRC cells. Glucose restriction might improve the effectiveness of classical chemotherapy against p53-positive CRC cells. The topoisomerase-1 inhibitor irinotecan and other chemotherapeutics that cause DNA damage induce metabolic adaptations in colorectal cancer (CRC) cells irrespective of their p53 status. Irinotecan enhances the glycolysis and oxygen consumption in CRC cells to deliver energy and biomolecules necessary for DNA repair and their survival. Compared to p53-deficient cells, p53-proficient CRC cells have a more active metabolism and use their intracellular metabolites more extensively. This metabolic switch creates a vulnerability to chemotherapy under glucose-restricted conditions for p53-positive cells.
    Language English
    Publishing date 2022-07-04
    Publishing country England
    Document type Journal Article
    ZDB-ID 2700141-6
    ISSN 2049-3002
    ISSN 2049-3002
    DOI 10.1186/s40170-022-00286-9
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  8. Article ; Online: Serine and Functional Metabolites in Cancer.

    Newman, Alice C / Maddocks, Oliver D K

    Trends in cell biology

    2017  Volume 27, Issue 9, Page(s) 645–657

    Abstract: Folate metabolism functions to supply one-carbon units that are vital for a range of biochemical reactions. Cancer cells can utilise serine as a major source of one-carbon units, rendering them dependent upon extracellular serine uptake or de novo serine ...

    Abstract Folate metabolism functions to supply one-carbon units that are vital for a range of biochemical reactions. Cancer cells can utilise serine as a major source of one-carbon units, rendering them dependent upon extracellular serine uptake or de novo serine synthesis for maximal growth and proliferation. One-carbon units are required for the production of critical cellular components, such as nucleotides, which enable cancer cells to maintain high proliferate rates. Of recent interest, one-carbon metabolism contributes to the biosynthesis and recycling of functional metabolites, such as ATP, S-adenosyl-methionine (SAM), and NAD(P)H, with important downstream consequences for cancer cell survival. In this review, we describe recent advances in our understanding of the importance of one-carbon metabolism in cancer, focussing upon the routes through which cancer cells obtain and use one-carbon units.
    MeSH term(s) Animals ; Carbon/metabolism ; Cell Proliferation/physiology ; Humans ; Neoplasms/metabolism ; Serine/metabolism
    Chemical Substances Serine (452VLY9402) ; Carbon (7440-44-0)
    Language English
    Publishing date 2017-06-07
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 30122-x
    ISSN 1879-3088 ; 0962-8924
    ISSN (online) 1879-3088
    ISSN 0962-8924
    DOI 10.1016/j.tcb.2017.05.001
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    Zs.A 3410: Show issues Location:
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  9. Article ; Online: One-carbon metabolism in cancer.

    Newman, Alice C / Maddocks, Oliver D K

    British journal of cancer

    2017  Volume 116, Issue 12, Page(s) 1499–1504

    Abstract: Cells require one-carbon units for nucleotide synthesis, methylation and reductive metabolism, and these pathways support the high proliferative rate of cancer cells. As such, anti-folates, drugs that target one-carbon metabolism, have long been used in ... ...

    Abstract Cells require one-carbon units for nucleotide synthesis, methylation and reductive metabolism, and these pathways support the high proliferative rate of cancer cells. As such, anti-folates, drugs that target one-carbon metabolism, have long been used in the treatment of cancer. Amino acids, such as serine are a major one-carbon source, and cancer cells are particularly susceptible to deprivation of one-carbon units by serine restriction or inhibition of de novo serine synthesis. Recent work has also begun to decipher the specific pathways and sub-cellular compartments that are important for one-carbon metabolism in cancer cells. In this review we summarise the historical understanding of one-carbon metabolism in cancer, describe the recent findings regarding the generation and usage of one-carbon units and explore possible future therapeutics that could exploit the dependency of cancer cells on one-carbon metabolism.
    MeSH term(s) Amino Acids/metabolism ; Carbon/metabolism ; Humans ; Metabolic Networks and Pathways ; Methylation ; NAD/biosynthesis ; NADP/biosynthesis ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Nucleotides/biosynthesis
    Chemical Substances Amino Acids ; Nucleotides ; NAD (0U46U6E8UK) ; NADP (53-59-8) ; Carbon (7440-44-0)
    Language English
    Publishing date 2017-05-04
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 80075-2
    ISSN 1532-1827 ; 0007-0920
    ISSN (online) 1532-1827
    ISSN 0007-0920
    DOI 10.1038/bjc.2017.118
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  10. Article ; Online: Use of

    Newman, Alice C / Labuschagne, Christiaan F / Vousden, Karen H / Maddocks, Oliver D K

    Methods in molecular biology (Clifton, N.J.)

    2019  Volume 1928, Page(s) 55–67

    Abstract: Tracing the fate of carbon-13 ( ...

    Abstract Tracing the fate of carbon-13 (
    MeSH term(s) Carbon Isotopes/metabolism ; Cell Line, Tumor ; Chromatography, Liquid ; DNA Methylation ; Epigenesis, Genetic ; Epigenomics/methods ; Humans ; Hydrolysis ; Methionine/metabolism ; Neoplasms/genetics ; Neoplasms/metabolism ; Nitrogen Isotopes/metabolism ; RNA/genetics ; RNA/metabolism ; Serine/metabolism ; Tandem Mass Spectrometry
    Chemical Substances Carbon Isotopes ; Nitrogen Isotopes ; Serine (452VLY9402) ; RNA (63231-63-0) ; Methionine (AE28F7PNPL) ; Carbon-13 (FDJ0A8596D)
    Language English
    Publishing date 2019-02-06
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-4939-9027-6_4
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