ArticleFunctional & integrative genomics2025
Investigating the impact of MCTP2 on immune suppression and drug resistance in glioblastoma.
Article in Functional & integrative genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Integrative multi-omics analysis and machine learning identify M2 macrophage-induced ferroptosis resistance in glioblastoma.Functional & integrative genomics · 2026Article
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The purpose of this study is to explore the role in MCTP2 glioblastoma (GBM) relapse and associated therapy target, especially its function on immune suppression together with drug-resistance. We performed transcriptional analysis of primary and recurrent GBM samples from the TCGA and CGGA databases to identify a key regulatory gene in relation to synaptic-related pathways using MCTP2. We used single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics analysis of expression in GBM samples to explore the population landscapes as well as tumor region-specific features at the molecular level. Functional studies via Western blotting, colony-formation assays and patient-derived organoid (PDO) models were used to assess the effect of MCTP2-depletion with/without SB52334 treatment in GBM. MCTP2 is significantly up-regulated in recurrent GBM and it correlates with poor survival. In addition, the increased expression of immune checkpoint markers PD-L1 (CD274) and CTLA-4 were significantly associated with high MCTP2 levels, indicating that MCTP2 could affect GBM patients' responses to anti-PD-1/PD-L1 or/and anti-CTLAs therapies. Overexpression of MCTP2 was also related to the increase in drug-resistance, specifically against SB52334. Combining MCTP2 KD with SB52334 significantly decreased primary cell clonogenic potential and organoid viability, suggesting a synergistic effect. MCTP2 plays a distinct role in GBM, acting as a novel facilitator of immune evasion and drug resistance with potential therapeutic implications. Our findings suggest that combining MCTP2 knockdown with SB52334 treatment could enhance the therapeutic efficacy against GBM.
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Registered trials
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