@prefix dcat: <http://www.w3.org/ns/dcat#> .
@prefix dct: <http://purl.org/dc/terms/> .
@prefix foaf: <http://xmlns.com/foaf/0.1/> .
@prefix vcard: <http://www.w3.org/2006/vcard/ns#> .
@prefix xsd: <http://www.w3.org/2001/XMLSchema#> .

<https://rec.harvest-normandie.data4citizen.com/dataset/oai-hal-tel-00912341v1> a dcat:Dataset ;
    dct:description """
              One of the hallmarks of cancer cells is to exhibit increased uptake and consumption of glucose.3-5% of the glucose entering into the cell leads to a minor pathway of the glucose metabolismknown as the hexosamine biosynthetic pathway (HBP). UDP-N-acetylglucosamine is the endproduct of HBP and is used as substrate by OGT (O-GlcNAc transferase) to modify diverserange of nuclear and cytoplasmic proteins with a recently characterized post-translationalmodification called O-GlcNAcylation. It corresponds to the addition of sugar moiety O-linked β-N-acetylglucosamine (O-GlcNAc) on serine or threonine residue of proteins. This process isantagonized by another enzyme called O-GlcNAcase (OGA). Recent studies indicated thepresence of increased O-GlcNAcylation level in several cancer cells. Moreover, inhibition ofOGT has been shown to reduce in vivo and in vitro tumor growth of breast cancer cells.However, the relationship between O-GlcNAcylation and the response to anti-cancer therapy hasnot been studied. Tamoxifen is the oldest and most prescribed selective-estrogen receptormodulator (SERM) for patients with estrogen receptor (ER)-positive breast cancer. Tamoxifen isknown to reduce tumor growth and invasion. Despite its beneficial effects de novo and acquiredresistance are great obstacles in its clinical effectiveness. We found that O-GlcNAc elevation inMCF-7 cells protected them from tamoxifen-induced cell death. Increased O-GlcNAc alsoincreased PI3-K/Akt signaling. However, the protective effect of PUGNAc+glucosamine fromtamoxifen-induced cell death is independent of PI3K/Akt pathway. Increased O-GlcNAcylationalso led to reduced ESR1 promoter activity and decreased expression of ERα at mRNA andprotein levels. The decrease in ERα expression is correlated with a reduced expression of twotamoxifen regulated genes i.e. early growth response 1 and p21 Waf1/Cip1. In conclusion, thisstudy showed for the first time the involvement of O-GlcNAcylation in reducing tamoxifen142sensitivity in MCF-7 cells. Thus, OGT can act as a novel therapeutic target for treatment oftamoxifen resistant cells.
            """ ;
    dct:identifier "NNT: 2013PA05T006" ;
    dct:issued "2026-05-08T00:20:40.322411"^^xsd:dateTime ;
    dct:language "en" ;
    dct:modified "2026-05-08T00:20:40.322415"^^xsd:dateTime ;
    dct:publisher <https://rec.harvest-normandie.data4citizen.com/organization/cce9db95-46d9-4dc2-84b6-764215d0a002> ;
    dct:title "Effect of O-GlcNAcylation on tamoxifen sensitivity in breast cancer derived MCF-7 cells" ;
    dcat:contactPoint [ a vcard:Organization ;
            vcard:fn "CCSD" ] ;
    dcat:distribution <https://rec.harvest-normandie.data4citizen.com/dataset/oai-hal-tel-00912341v1/resource/f63b3e06-d301-44e5-9d18-077dcccd5847> ;
    dcat:keyword "cancer-du-sein",
        "infoeu-reposemanticsdoctoralthesis",
        "o-glcnacylation",
        "sdvsalife-sciences-q-bioagricultural-sciences",
        "theses" ;
    dcat:landingPage <https://theses.hal.science/tel-00912341> .

<https://rec.harvest-normandie.data4citizen.com/dataset/oai-hal-tel-00912341v1/resource/f63b3e06-d301-44e5-9d18-077dcccd5847> a dcat:Distribution ;
    dct:format "HTML" ;
    dct:issued "2026-05-08T00:20:40.323968"^^xsd:dateTime ;
    dct:modified "2026-05-08T00:20:40.315038"^^xsd:dateTime ;
    dct:title "Effect of O-GlcNAcylation on tamoxifen sensitivity in breast cancer derived MCF-7 cells" ;
    dcat:accessURL <https://theses.hal.science/tel-00912341> .

<https://rec.harvest-normandie.data4citizen.com/organization/cce9db95-46d9-4dc2-84b6-764215d0a002> a foaf:Agent ;
    foaf:name "test_moissonnage_selune" .

<https://theses.hal.science/tel-00912341> a foaf:Document .

