FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4313857781> ?p ?o ?g. }

• W4313857781 abstract "The immune regulator galectin-9 (Gal-9) is commonly involved in the regulation of cell proliferation, but with various impacts depending on the cell type. Here, we revealed that Gal-9 expression was persistently increased in Epstein-Barr virus (EBV)-infected primary B cells from the stage of early infection to the stage of mature lymphoblastoid cell lines (LCLs). This sustained upregulation paralleled that of gene sets related to cell proliferation, such as oxidative phosphorylation, cell cycle activation, and DNA replication. Knocking down or blocking Gal-9 expression obstructed the establishment of latent infection and outgrowth of EBV-infected B cells, while exogenous Gal-9 protein promoted EBV acute and latent infection and outgrowth of EBV-infected B cells at the early infection stage. Mechanically, stimulator of interferon gene (STING) activation or signal transducer and activator of transcription 3 (STAT3) inhibition impeded the outgrowth of EBV-infected B cells and promotion of Gal-9-induced lymphoblastoid cell line (LCL) transformation. Accordingly, Gal-9 expression was upregulated by forced EBV nuclear antigen 1 (EBNA1) expression in 293T cells in vitro. Clinical data showed that Gal-9 expression in B-cell lymphomas (BCLs) correlated positively with EBNA1 and disease stage. Targeting Gal-9 slowed LCL tumor growth and metastasis in xenografted immunodeficient mice. These findings highlight an oncogenic role of Gal-9 in EBV-associated BCLs, indicating that Gal-9 boosts the transformation of EBV-infected B cells. IMPORTANCE The cross talk between Epstein-Barr virus (EBV) and the host cell transcriptome assumes important roles in the oncogenesis of EBV-associated malignancies. Here, we first observed that endogenous Gal-9 expression was persistently increased along with an overturned V-type change in antivirus signaling during the immortalization of EBV-transformed B cells. Upregulation of Gal-9 promoted the outgrowth and latent infection of EBV-infected B cells, which was linked to B-cell-origin tumors by suppressing STING signaling and subsequently promoting STAT3 phosphorylation. EBV nuclear antigen EBNA1 induced Gal-9 expression and formed a positive feedback loop with Gal-9 in EBV-infected B cells. Tumor Gal-9 levels were positively correlated with disease stage and EBNA1 expression in patients with B-cell lymphomas (BCLs). Targeting Gal-9 slowed the growth and metastases of LCL tumors in immunodeficient mice. Altogether, our findings indicate that Gal-9 is involved in the lymphomagenesis of EBV-positive BCLs through cross talk with EBNA1 and STING signals." @default.
• W4313857781 created "2023-01-10" @default.
• W4313857781 creator A5001015133 @default.
• W4313857781 creator A5017951781 @default.
• W4313857781 creator A5034488277 @default.
• W4313857781 creator A5063414905 @default.
• W4313857781 creator A5073843820 @default.
• W4313857781 creator A5077242837 @default.
• W4313857781 creator A5078398526 @default.
• W4313857781 creator A5083967189 @default.
• W4313857781 creator A5085756337 @default.
• W4313857781 date "2023-02-14" @default.
• W4313857781 modified "2023-10-14" @default.
• W4313857781 title "Galectin-9 Facilitates Epstein-Barr Virus Latent Infection and Lymphomagenesis in Human B Cells" @default.
• W4313857781 cites W1624270294 @default.
• W4313857781 cites W1638424324 @default.
• W4313857781 cites W1681696483 @default.
• W4313857781 cites W1961662530 @default.
• W4313857781 cites W1966831463 @default.
• W4313857781 cites W1968791512 @default.
• W4313857781 cites W1974053860 @default.
• W4313857781 cites W1982929042 @default.
• W4313857781 cites W2002525330 @default.
• W4313857781 cites W2009432847 @default.
• W4313857781 cites W2025581632 @default.
• W4313857781 cites W2041345682 @default.
• W4313857781 cites W2044702473 @default.
• W4313857781 cites W2068128836 @default.
• W4313857781 cites W2070631889 @default.
• W4313857781 cites W2071311981 @default.
• W4313857781 cites W2088103993 @default.
• W4313857781 cites W2113704699 @default.
• W4313857781 cites W2128179579 @default.
• W4313857781 cites W2132413371 @default.
• W4313857781 cites W2139674860 @default.
• W4313857781 cites W2152358904 @default.
• W4313857781 cites W2159090549 @default.
• W4313857781 cites W2162538131 @default.
• W4313857781 cites W2299059283 @default.
• W4313857781 cites W2475074325 @default.
• W4313857781 cites W2606869403 @default.
• W4313857781 cites W2738453388 @default.
• W4313857781 cites W2783034964 @default.
• W4313857781 cites W2796612507 @default.
• W4313857781 cites W2801911828 @default.
• W4313857781 cites W2887302504 @default.
• W4313857781 cites W2888204442 @default.
• W4313857781 cites W2895561458 @default.
• W4313857781 cites W2917427311 @default.
• W4313857781 cites W2919692138 @default.
• W4313857781 cites W2920237528 @default.
• W4313857781 cites W2929108602 @default.
• W4313857781 cites W2941393885 @default.
• W4313857781 cites W2948703807 @default.
• W4313857781 cites W2949088564 @default.
• W4313857781 cites W3001605540 @default.
• W4313857781 cites W3010193287 @default.
• W4313857781 cites W3015197653 @default.
• W4313857781 cites W3038807442 @default.
• W4313857781 cites W3038995504 @default.
• W4313857781 cites W3131347681 @default.
• W4313857781 cites W3137380802 @default.
• W4313857781 cites W3152326806 @default.
• W4313857781 cites W3155357417 @default.
• W4313857781 doi "https://doi.org/10.1128/spectrum.04932-22" @default.
• W4313857781 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36622166" @default.
• W4313857781 hasPublicationYear "2023" @default.
• W4313857781 type Work @default.
• W4313857781 citedByCount "1" @default.
• W4313857781 countsByYear W43138577812023 @default.
• W4313857781 crossrefType "journal-article" @default.
• W4313857781 hasAuthorship W4313857781A5001015133 @default.
• W4313857781 hasAuthorship W4313857781A5017951781 @default.
• W4313857781 hasAuthorship W4313857781A5034488277 @default.
• W4313857781 hasAuthorship W4313857781A5063414905 @default.
• W4313857781 hasAuthorship W4313857781A5073843820 @default.
• W4313857781 hasAuthorship W4313857781A5077242837 @default.
• W4313857781 hasAuthorship W4313857781A5078398526 @default.
• W4313857781 hasAuthorship W4313857781A5083967189 @default.
• W4313857781 hasAuthorship W4313857781A5085756337 @default.
• W4313857781 hasBestOaLocation W43138577811 @default.
• W4313857781 hasConcept C104317684 @default.
• W4313857781 hasConcept C1491633281 @default.
• W4313857781 hasConcept C159047783 @default.
• W4313857781 hasConcept C159654299 @default.
• W4313857781 hasConcept C171958077 @default.
• W4313857781 hasConcept C203014093 @default.
• W4313857781 hasConcept C2522874641 @default.
• W4313857781 hasConcept C2778453870 @default.
• W4313857781 hasConcept C2778923194 @default.
• W4313857781 hasConcept C2781375147 @default.
• W4313857781 hasConcept C29537977 @default.
• W4313857781 hasConcept C502942594 @default.
• W4313857781 hasConcept C54355233 @default.
• W4313857781 hasConcept C555283112 @default.
• W4313857781 hasConcept C62112901 @default.
• W4313857781 hasConcept C62478195 @default.
• W4313857781 hasConcept C81885089 @default.
• W4313857781 hasConcept C86803240 @default.
• W4313857781 hasConcept C95444343 @default.

• next