ArticleAging2022
The immune regulation of BCL3 in glioblastoma with mutated IDH1.
Article in Aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Current progress of anti‑PD‑1/PDL1 immunotherapy for glioblastoma (Review).Molecular medicine reports · 2024Review
- Multifaceted roles for BCL3 in cancer: a proto-oncogene comes of age.Molecular cancer · 2024Review
- LC-MS/MS-Based Proteomics Approach for the Identification of Candidate Serum Biomarkers in Patients with Narcolepsy Type 1.Biomolecules · 2023Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlioblastoma in the brain is the most malignant solid tumor with a poor prognosis. Screening critical targets and exploring underlying mechanisms will be a benefit for diagnoses and treatment. IDH1 mutation (R132) was used to distinguish glioblastoma grade and predict prognosis as a significant marker. However, the manner of IDH1 mutation regulating glioblastoma development was still unclear.
methodsTo study the function of IDH1 mutation, multi-type sequencing data (transcriptome, methylation and copy number variation) from the GEO and TCGA database were analyzed using bioinformatics techniques. The biological functions of IDH1 mutation (R132) would be comprehensively evaluated from the regulatory networks, tumor immune microenvironment and clinical relevance. Then the analysis result would be validated by experimental techniques.
resultsCompared with adjacent tissues, IDH1 was up-regulated in glioblastoma, which also positively correlated with the malignant degree and a poor prognosis. To further study the mechanism of mutated IDH1 (R132) function, 5 correlated genes (FABP5, C1RL, MIR155HG, CSTA and BCL3) were identified by different expression gene screening, enrichment analysis and network construction successively. Among them, the BCL3 was a transcription factor that may induce IDH1expression. Through calculating the correlation coefficient, it was found that in IDH1
conclusionsIDH1 may participate in pathological mechanisms of glioblastoma via expression alteration or gene mutation. Furthermore, IDH1 mutation might improve prognosis via suppressing the expression of FABP5, C1RL, MIR155HG, CSTA and BCL3. Meanwhile, it was identified that BCL3 might perform similar immunomodulatory functions with IDH1 as an upstream transcript factor.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.