LINC01088 prevents ferroptosis in glioblastoma by enhancing SLC7A11 via HLTF/USP7 axis DOI Creative Commons
Yujie Zhou,

Zhen Zhao,

Jiang Cheng

и другие.

Clinical and Translational Medicine, Год журнала: 2025, Номер 15(3)

Опубликована: Фев. 25, 2025

Glioblastoma multiforme (GBM)is a highly aggressive malignancy of the central nervous system characterized by poor survival rates. Ferroptosis, an iron-dependent cell death pathway, is promising therapeutic target for GBM. However, current treatments targeting pathways have not yielded expected results. Long noncoding RNAs (lncRNAs) been implicated in tumour proliferation, however, their role ferroptosis GBM remains underexplored. This study investigated interplay between lncRNA LINC01088 and to identify novel strategies. We conducted gain- loss-of-function studies assess impact on tumourigenesis both vitro vivo. Bioinformatics, dual-luciferase reporter assays, chromatin immunoprecipitation, RNA pulldown, mass spectrometry, immunoprecipitation (RIP), transcriptome sequencing were utilized elucidate mechanisms underlying expression its downstream effects ferroptosis. The transcription factor specificity protein 1 (SP1) was identified as promoter transcription, which facilitated progression. found inhibit promote malignancy. Mechanistically, stabilized HLTF enhancing interaction with USP7 preventing ubiquitin-mediated degradation. stabilization led upregulation SLC7A11, inhibits Rescue experiments confirmed that altering levels reversed ferroptotic phenotypes associated modulation. revealed SP1/LINC01088/HLTF/USP7/SLC7A11 axis regulates GBM, highlighting potential ferroptosis-dependent treatment. transcriptionally upregulated SP1. acts scaffold platform bind HLTF. USP7, deubiquitinating enzyme HLTF, participates inhibiting ubiquitin-proteasome degradation upregates cells inhibited.

Язык: Английский

LINC01088 prevents ferroptosis in glioblastoma by enhancing SLC7A11 via HLTF/USP7 axis DOI Creative Commons
Yujie Zhou,

Zhen Zhao,

Jiang Cheng

и другие.

Clinical and Translational Medicine, Год журнала: 2025, Номер 15(3)

Опубликована: Фев. 25, 2025

Glioblastoma multiforme (GBM)is a highly aggressive malignancy of the central nervous system characterized by poor survival rates. Ferroptosis, an iron-dependent cell death pathway, is promising therapeutic target for GBM. However, current treatments targeting pathways have not yielded expected results. Long noncoding RNAs (lncRNAs) been implicated in tumour proliferation, however, their role ferroptosis GBM remains underexplored. This study investigated interplay between lncRNA LINC01088 and to identify novel strategies. We conducted gain- loss-of-function studies assess impact on tumourigenesis both vitro vivo. Bioinformatics, dual-luciferase reporter assays, chromatin immunoprecipitation, RNA pulldown, mass spectrometry, immunoprecipitation (RIP), transcriptome sequencing were utilized elucidate mechanisms underlying expression its downstream effects ferroptosis. The transcription factor specificity protein 1 (SP1) was identified as promoter transcription, which facilitated progression. found inhibit promote malignancy. Mechanistically, stabilized HLTF enhancing interaction with USP7 preventing ubiquitin-mediated degradation. stabilization led upregulation SLC7A11, inhibits Rescue experiments confirmed that altering levels reversed ferroptotic phenotypes associated modulation. revealed SP1/LINC01088/HLTF/USP7/SLC7A11 axis regulates GBM, highlighting potential ferroptosis-dependent treatment. transcriptionally upregulated SP1. acts scaffold platform bind HLTF. USP7, deubiquitinating enzyme HLTF, participates inhibiting ubiquitin-proteasome degradation upregates cells inhibited.

Язык: Английский

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