ArticleNeuro-oncology2024
Copy number gain of FAM131B-AS2 promotes the progression of glioblastoma by mitigating replication stress.
Article in Neuro-oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- IL-17D reprograms CD93Cellular & molecular immunology · 2026Article
- Identification ofBiomedicines · 2026Article
- Predicting Clinical Prognosis and Treatment Response in Glioblastoma Based on Gene Replication Stress-Related Features.Current medicinal chemistry · 2026Article
- Long non-coding RNAs in glioblastoma: from molecular drivers to therapeutic targets.Frontiers in immunology · 2026Review
- STING signaling pathway: An oasis in the glioblastoma immune desert.Theranostics · 2026Review
- Targeting non-coding RNAs to overcome resistance and improving outcomes in glioblastoma.Global medical genetics · 2025Review
- Dual roles of LncRNA RNA143598: a biomarker for rheumatoid arthritis and its implications in cancer.Clinical rheumatology · 2025Article
- The STING Signaling: A Novel Target for Central Nervous System Diseases.Cellular and molecular neurobiology · 2025Review
- Deciphering novel mitochondrial signatures: multi-omics analysis uncovers cross-disease markers and oligodendrocyte pathways in Alzheimer's disease and glioblastoma.Frontiers in aging neuroscience · 2025Article
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Authors and funding
11 authors.
Funding
Abstract
backgroundGlioblastoma (GBM) is characterized by chromosome 7 copy number gains, notably 7q34, potentially contributing to therapeutic resistance, yet the underlying oncogenes have not been fully characterized. Pertinently, the significance of long noncoding RNAs (lncRNAs) in this context has gained attention, necessitating further exploration.
methodsFAM131B-AS2 was quantified in GBM samples and cells using qPCR. Overexpression and knockdown of FAM131B-AS2 in GBM cells were used to study its functions in vivo and in vitro. The mechanisms of FAM131B-AS2 were studied using RNA-seq, qPCR, Western blotting, RNA pull-down, coimmunoprecipitation assays, and mass spectrometry analysis. The phenotypic changes that resulted from FAM131B-AS2 variation were evaluated through CCK8 assay, EdU assay, comet assay, and immunofluorescence.
resultsOur analysis of 149 primary GBM patients identified FAM131B-AS2, a lncRNA located in the 7q34 region, whose upregulation predicts poor survival. Mechanistically, FAM131B-AS2 is a crucial regulator of the replication stress response, stabilizing replication protein A1 through recruitment of ubiquitin-specific peptidase 7 and activating the ataxia telangiectasia and rad3-related protein kinase pathway to protect single-stranded DNA from breakage. Furthermore, FAM131B-AS2 overexpression inhibited CD8+ T-cell infiltration, while FAM131B-AS2 inhibition activated the cGAS-STING pathway, increasing lymphocyte infiltration and improving the response to immune checkpoint inhibitors.
conclusionsFAM131B-AS2 emerges as a promising indicator for adjuvant therapy response and could also be a viable candidate for combined immunotherapies against GBMs.
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