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  1. AU="Zhou, Qinyao"
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  1. Artikel ; Online: tRF-29-79 regulates lung adenocarcinoma progression through mediating glutamine transporter SLC1A5.

    Shi, Yuanjian / Pan, Zehao / Feng, Yipeng / Zhou, Qinyao / Wang, Qinglin / Wang, Hui / Dong, Gaochao / Xia, Wenjie / Jiang, Feng

    Carcinogenesis

    2024  

    Abstract: In recent decades, considerable evidence has emerged indicating the involvement of tRNA-derived fragments (tRFs) in cancer progression through various mechanisms. However, the biological effects and mechanisms of tRFs in lung adenocarcinoma (LUAD) remain ...

    Abstract In recent decades, considerable evidence has emerged indicating the involvement of tRNA-derived fragments (tRFs) in cancer progression through various mechanisms. However, the biological effects and mechanisms of tRFs in lung adenocarcinoma (LUAD) remain unclear. In this study, we screen out tRF-29-79, a 5'-tRF derived from tRNAGlyGCC, through profiling the tRF expressions in three pairs of LUAD tissues. We show that tRF-29-79 is down-regulated in LUAD and down-regulation of tRF-29-79 is associated with poorer prognosis. In vivo and in vitro assay reveal that tRF-29-79 inhibits proliferation, migration, and invasion of LUAD cells. Mechanistically, we discovered that tRF-29-79 interacts with the RNA-binding protein PTBP1 and facilitates the transportation of PTBP1 from nucleus to cytoplasm, which regulates alternative splicing in the 3' untranslated region (UTR) of SLC1A5 pre-mRNA. Given that SLC1A5 is a core transporter of glutamine, we proved that tRF-29-79 mediate glutamine metabolism of LUAD through affecting the stability of SLC1A5 mRNA, thus exerts its anticancer function. In summary, our findings uncover the novel mechanism that tRF-29-79 participates in glutamine metabolism through interacting with PTBP1 and regulating alternative splicing in the 3' UTR of SLC1A5 pre-mRNA.
    Sprache Englisch
    Erscheinungsdatum 2024-02-15
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 603134-1
    ISSN 1460-2180 ; 0143-3334
    ISSN (online) 1460-2180
    ISSN 0143-3334
    DOI 10.1093/carcin/bgae010
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: The heparan sulfate mimetic Muparfostat aggravates steatohepatitis in obese mice due to its binding affinity to lipoprotein lipase.

    Zhang, Jia / Li, Kai / Sun, Hao-Ran / Sun, Shao-Kun / Zhu, Ya-Ting / Ge, Yu-Ting / Wu, Yu-Xuan / Zhou, Qin-Yao / Li, Guan-Ting / Chang, Xiao-Ai / Sun, Peng / Ding, Ying / Han, Xiao

    British journal of pharmacology

    2023  Band 180, Heft 14, Seite(n) 1803–1818

    Abstract: Background and purpose: Heparanase is the only confirmed endoglycosidase that cleaves heparan sulfate (HS), a ubiquitous glycosaminoglycan with various essential roles in multiple pathological processes. Thus, the development of heparanase inhibitors ... ...

    Abstract Background and purpose: Heparanase is the only confirmed endoglycosidase that cleaves heparan sulfate (HS), a ubiquitous glycosaminoglycan with various essential roles in multiple pathological processes. Thus, the development of heparanase inhibitors has become an attractive strategy for drug discovery, especially in tumour therapy, in which HS mimetics are the most promising compounds. The various biological effects of heparanase also suggest a role for HS mimetics in many non-cancer indications, such as type 1 diabetes. However, the potential benefits of HS mimetics in obesity-related type 2 diabetes have not been elucidated.
    Experimental approach: In this study, we investigated muparfostat (PI-88), a developed HS mimetic currently enrolled in Phase III clinical trials, in obese mouse models and in vitro cultured murine hepatocytes.
    Key results: Daily administration of muparfostat for 4 weeks caused hyperlipidaemia and aggravated hepatic steatosis in obese mice models, but not in lean animals. In cultured hepatocytes, muparfostat did not alter lipid accumulation. Acute tests suggested that muparfostat binds to lipoprotein lipase in competition with HS on vascular endothelial cell surfaces, thereby reducing the degradation of circulating triglycerides by lipoprotein lipase and subsequent uptake of fatty acids into vascular endothelial cells and causing hyperlipidaemia. This hyperlipidaemia aggravates hepatic steatosis and causes liver injury in muparfostat-treated obese mice.
    Conclusions and implications: The binding activity of HS mimetics to lipoprotein lipase should be investigated as an additional pharmacological effect during heparanase inhibitor drug discovery. This study also provides novel evidence for an increased risk of drug-induced liver injury in obese individuals.
    Mesh-Begriff(e) Animals ; Mice ; Diabetes Mellitus, Type 2 ; Endothelial Cells/metabolism ; Fatty Liver ; Heparitin Sulfate ; Lipoprotein Lipase/metabolism ; Mice, Obese
    Chemische Substanzen Heparitin Sulfate (9050-30-0) ; Lipoprotein Lipase (EC 3.1.1.34) ; phosphomannopentaose sulfate
    Sprache Englisch
    Erscheinungsdatum 2023-02-20
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80081-8
    ISSN 1476-5381 ; 0007-1188
    ISSN (online) 1476-5381
    ISSN 0007-1188
    DOI 10.1111/bph.16047
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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