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Updated: Aug 6, 2026

A Reporter Based Cellular Assay for Monitoring Splicing Efficiency
Published on: September 15, 2021
The spliceosome component SNRPC promotes glioma progression by sustaining mitochondrial function and TNFAIP2
Peng Ma1,2, Jiang Wu3, Zhen Ma2
1Department of Neurosurgery, The Third Affiliated Hospital of Soochow University, Changzhou, China.
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.
Insights
Small nuclear ribonucleoprotein C (SNRPC) drives glioma malignancy by impairing mitochondrial function and increasing proliferation. Targeting SNRPC offers a novel therapeutic strategy for this aggressive brain tumor.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Human glioma is an aggressive brain tumor with poor outcomes, requiring new therapeutic targets.
- The spliceosome component SNRPC is linked to cancer but its role in glioma is unknown.
Purpose of the Study:
- To investigate the expression, function, and mechanisms of SNRPC in human glioma.
- To determine if SNRPC is a potential therapeutic target for glioma.
Main Methods:
- Bioinformatic analysis of SNRPC expression in glioma tissues and correlation with clinical data.
- Functional studies using SNRPC knockdown (shRNA) and knockout (CRISPR/Cas9) in glioma cells.
- Investigation of SNRPC's role in mitochondrial metabolism, cell cycle, apoptosis, and oncogene expression (TNFAIP2).
- In vivo studies using subcutaneous and orthotopic glioma xenograft models.
Main Results:
- SNRPC is upregulated in glioma, correlating with higher grade, aggressive subtypes, and poor prognosis.
- SNRPC silencing/knockout inhibits glioma cell proliferation, migration, invasion, and induces cell cycle arrest and apoptosis.
- SNRPC loss causes mitochondrial dysfunction (impaired respiration, ATP depletion, ROS production).
- SNRPC regulates TNFAIP2 expression, promoting malignant phenotypes.
- SNRPC knockdown/knockout suppresses tumor growth in vivo.
Conclusions:
- SNRPC is a key driver of glioma malignancy, sustaining mitochondrial hyperfunction and promoting proliferation.
- SNRPC is a potential prognostic biomarker and therapeutic target for human glioma.
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