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  1. Article ; Online: The metabolic contribution of SKN-1/Nrf2 to the lifespan of Caenorhabditis elegans.

    Phan, Hong-Duc / Nguyen, Tin Tin Manh / Lee, Sujin / Seo, Munjun / An, Yong Jin / de Guzman, Arvie Camille V

    Metabolomics : Official journal of the Metabolomic Society

    2023  Volume 19, Issue 6, Page(s) 58

    Abstract: Background and aims: SKN-1, a C. elegans transcription factor analogous to the mammalian NF-E2-related factor (Nrf2), has been known to promote oxidative stress resistance aiding nematodes' longevity. Although SKN-1's functions suggest its implication ... ...

    Abstract Background and aims: SKN-1, a C. elegans transcription factor analogous to the mammalian NF-E2-related factor (Nrf2), has been known to promote oxidative stress resistance aiding nematodes' longevity. Although SKN-1's functions suggest its implication in lifespan modulation through cellular metabolism, the actual mechanism of how metabolic rearrangements contribute to SKN-1's lifespan modulation has yet to be well characterized. Therefore, we performed the metabolomic profiling of the short-lived skn-1-knockdown C. elegans.
    Methods: We analyzed the metabolic profile of the skn-1-knockdown worms with nuclear magnetic resonance (NMR) spectroscopy and liquid chromatography-tandem mass spectrometry (LC-MS/MS) and obtained distinctive metabolomic profiles compared to WT worms. We further extended our study with gene expression analysis to examine the expression level of genes encoding all metabolic enzymes.
    Results: A significant increase in the phosphocholine and AMP/ATP ratio, potential biomarkers of aging, was observed, accompanied by a decrease in the transsulfuration metabolites, NADPH/NADP
    Conclusion: Our multi-omics results consistently revealed that the cytoprotective mechanisms, including cellular redox reactions and xenobiotic detoxification system, contribute to the roles of SKN-1/Nrf2 in the lifespan of worms.
    MeSH term(s) Animals ; Acetaminophen/metabolism ; Caenorhabditis elegans/metabolism ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; Chromatography, Liquid ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Glutathione/metabolism ; Longevity/genetics ; Mammals/metabolism ; Metabolomics ; NADP/metabolism ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Tandem Mass Spectrometry
    Chemical Substances Acetaminophen (362O9ITL9D) ; Caenorhabditis elegans Proteins ; DNA-Binding Proteins ; Glutathione (GAN16C9B8O) ; NADP (53-59-8) ; NF-E2-Related Factor 2 ; skn-1 protein, C elegans (148733-36-2)
    Language English
    Publishing date 2023-06-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2250617-2
    ISSN 1573-3890 ; 1573-3882
    ISSN (online) 1573-3890
    ISSN 1573-3882
    DOI 10.1007/s11306-023-02022-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6361: Show issues Location:
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  2. Article ; Online: Real-Time Monitoring of Host-Gut Microbial Interspecies Interaction in Anticancer Drug Metabolism.

    Nguyen, Tin Tin Manh / Mai, Van-Hieu / Kim, Han Sun / Kim, Doyeon / Seo, Munjun / An, Yong Jin / Park, Sunghyouk

    Journal of the American Chemical Society

    2022  Volume 144, Issue 19, Page(s) 8529–8535

    Abstract: Gut microbiome can affect drug metabolism considerably, leading to modified drug response. However, quantitative estimation of host vs. microbial contributions in a living host-gut microbiome system has been challenging. Using the interspecies system ... ...

    Abstract Gut microbiome can affect drug metabolism considerably, leading to modified drug response. However, quantitative estimation of host vs. microbial contributions in a living host-gut microbiome system has been challenging. Using the interspecies system of
    MeSH term(s) Antineoplastic Agents/metabolism ; Antineoplastic Agents/pharmacology ; Bacteria/metabolism ; Fluorouracil/pharmacology ; Gastrointestinal Microbiome ; Humans ; RNA, Ribosomal, 16S/genetics ; RNA, Ribosomal, 16S/metabolism
    Chemical Substances Antineoplastic Agents ; RNA, Ribosomal, 16S ; Fluorouracil (U3P01618RT)
    Language English
    Publishing date 2022-05-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3155-0
    ISSN 1520-5126 ; 0002-7863
    ISSN (online) 1520-5126
    ISSN 0002-7863
    DOI 10.1021/jacs.1c10998
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Bonn / Germany

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  3. Article ; Online: GPX8 regulates clear cell renal cell carcinoma tumorigenesis through promoting lipogenesis by NNMT.

    Nguyen, Tin Tin Manh / Nguyen, Thi Ha / Kim, Han Sun / Dao, Thien T P / Moon, Yechan / Seo, Munjun / Kang, Sunmi / Mai, Van-Hieu / An, Yong Jin / Jung, Cho-Rok / Kim, Jin-Mo / Park, Sunghyouk

    Journal of experimental & clinical cancer research : CR

    2023  Volume 42, Issue 1, Page(s) 42

    Abstract: Background: Clear cell renal cell carcinoma (ccRCC), with its hallmark phenotype of high cytosolic lipid content, is considered a metabolic cancer. Despite the implication of this lipid-rich phenotype in ccRCC tumorigenesis, the roles and regulators of ... ...

    Abstract Background: Clear cell renal cell carcinoma (ccRCC), with its hallmark phenotype of high cytosolic lipid content, is considered a metabolic cancer. Despite the implication of this lipid-rich phenotype in ccRCC tumorigenesis, the roles and regulators of de novo lipid synthesis (DNL) in ccRCC remain largely unexplained.
    Methods: Our bioinformatic screening focused on ccRCC-lipid phenotypes identified glutathione peroxidase 8 (GPX8), as a clinically relevant upstream regulator of DNL. GPX8 genetic silencing was performed with CRISPR-Cas9 or shRNA in ccRCC cell lines to dissect its roles. Untargeted metabolomics, RNA-seq analyses, and other biochemical assays (e.g., lipid droplets staining, fatty acid uptake, cell proliferation, xenograft, etc.) were carried out to investigate the GPX8's involvement in lipid metabolism and tumorigenesis in ccRCC. The lipid metabolic function of GPX8 and its downstream were also measured by isotope-tracing-based DNL flux measurement.
    Results: GPX8 knockout or downregulation substantially reduced lipid droplet levels (independent of lipid uptake), fatty acid de novo synthesis, triglyceride esterification in vitro, and tumor growth in vivo. The downstream regulator was identified as nicotinamide N-methyltransferase (NNMT): its knockdown phenocopied, and its expression rescued, GPX8 silencing both in vitro and in vivo. Mechanically, GPX8 regulated NNMT via IL6-STAT3 signaling, and blocking this axis suppressed ccRCC survival by activating AMPK. Notably, neither the GPX8-NNMT axis nor the DNL flux was affected by the von Hippel Lindau (VHL) status, the conventional regulator of ccRCC high lipid content.
    Conclusions: Taken together, our findings unravel the roles of the VHL-independent GPX8-NNMT axis in ccRCC lipid metabolism as related to the phenotypes and growth of ccRCC, which may be targeted for therapeutic purposes.
    MeSH term(s) Humans ; Carcinoma, Renal Cell/pathology ; Lipogenesis ; Cell Transformation, Neoplastic/genetics ; Carcinogenesis/genetics ; Carcinoma/genetics ; Kidney Neoplasms/pathology ; Lipids ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Nicotinamide N-Methyltransferase/genetics ; Nicotinamide N-Methyltransferase/metabolism ; Peroxidases/genetics ; Peroxidases/metabolism
    Chemical Substances Lipids ; NNMT protein, human (EC 2.1.1.1) ; Nicotinamide N-Methyltransferase (EC 2.1.1.1) ; GPX8 protein, human (EC 1.11.1.-) ; Peroxidases (EC 1.11.1.-)
    Language English
    Publishing date 2023-02-07
    Publishing country England
    Document type Journal Article
    ZDB-ID 803138-1
    ISSN 1756-9966 ; 0392-9078
    ISSN (online) 1756-9966
    ISSN 0392-9078
    DOI 10.1186/s13046-023-02607-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2065: Show issues Location:
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    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
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