ArticleThe Indian journal of medical research2025
IL-32-mediated caspase-43 induction: Shaping macrophage differentiation & immunomodulation in glioblastoma multiforme.
Article in The Indian journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background & objectives Glioblastoma multiforme (GBM) is the most aggressive form of brain tumour, characterised by rapid progression, high recurrence, and poor prognosis. The immunosuppressive tumour microenvironment (TME) of GBM poses a major barrier to effective therapy. Interleukin (IL)-32, a pro-inflammatory cytokine, has been implicated in cancer progression, but its specific role in GBM remains unclear. This study aimed to investigate the immunoregulatory functions of IL-32 in GBM, particularly its impact on monocyte differentiation and macrophage polarisation. Methods Transcriptomic data from TCGA-GBM and GEO-GSE156902 were analysed to identify differentially expressed genes (DEGs), with a focus on IL-32. Functional enrichment analyses (GO and Kyoto Encyclopaedia of Genes and Genomes- KEGG) and protein-protein interaction (PPI) network construction were conducted using R software and Cytoscape. IL-32 expression was validated by qPCR and Western blot (WB) in GBM cell lines. Single-cell RNA sequencing data were integrated to determine IL-32 expression across brain cell types. Additionally, correlations between IL-32 and RNA modification genes (m6A, m5C, m1A) were analysed. Results IL-32 was significantly upregulated in GBM tissues and particularly enriched in microglial cells. Functional studies revealed that IL-32 promotes caspase-43-mediated monocyte differentiation into macrophages. Moreover, IL-32 induced a phenotypic shift from M1 to M2 macrophages via NF-κB pathway activation. PPI analysis confirmed IL-32 as a hub gene involved in immune regulation. RNA modification analysis showed positive correlations between IL-32 and METTL3, and a negative correlation with TET2, indicating epigenetic modulation of IL-32-related immune functions. Interpretation & conclusions IL-32 plays a pivotal immunoregulatory role in the GBM microenvironment by driving macrophage differentiation and M2 polarisation, contributing to tumour immune evasion. These findings highlight IL-32 as a potential therapeutic target for modulating immune responses in GBM and underscore its relevance in the design of future immunotherapeutic strategies.
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