ArticleCell death & disease2026
The spliceosome component SNRPC promotes glioma progression by sustaining mitochondrial function and TNFAIP2 signaling.
Article in Cell death & disease, 2026. 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
Human glioma is a devastating primary brain tumor with a dismal prognosis, necessitating the identification of novel therapeutic targets. The small nuclear ribonucleoprotein C (SNRPC), a core spliceosome component, is implicated in cancer, but its role in glioma remains unexplored. This study aimed to delineate the expression, function, and underlying mechanisms of SNRPC in human glioma. The bioinformatic analysis revealed that SNRPC is significantly upregulated in glioma tissues, with expression levels correlating strongly with higher tumor grade, aggressive molecular subtypes (IDH wild-type, 1p/19q non-codeleted), and poor patient prognosis, establishing it as a robust independent biomarker. Single-cell analysis pinpointed SNRPC enrichment in malignant glioma cells, and co-expression studies linked it to mitochondrial metabolism and oxidative phosphorylation. SNRPC expression is also upregulated in locally-resected glioma tissues and various glioma cell types. Functionally, silencing (by targeted shRNA) or knocking out (via CRISPR/Cas9 method) of SNRPC profoundly attenuated glioma cell proliferation, migration, and invasion, while inducing G1-S arrest and apoptosis. These effects were specifically observed in malignant glioma cells, sparing normal astrocytes. Mechanistically, loss of SNRPC led to severe mitochondrial dysfunction, characterized by impaired mitochondrial respiration, ATP depletion, membrane depolarization, and excessive ROS (reactive oxygen species) production. Conversely, SNRPC overexpression enhanced mitochondrial bioenergetics and promoted malignant phenotypes. SNRPC promoted glioma malignancy by regulating the expression of a key oncogene tumor necrosis factor alpha-induced protein 2 (TNFAIP2), which acts as a key downstream effector to drive increased cell proliferation and migration. Critically, SNRPC knockdown suppressed subcutaneous glioma xenograft growth and disrupted mitochondrial bioenergetics. Its knockout also impeded the intracranial glioma growth in an orthotopic mouse model. Our findings establish SNRPC as a pivotal driver of glioma malignancy by sustaining mitochondrial hyperfunction and TNFAIP2 expression essential for tumor cell proliferation.
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