ArticleScientific reports2026
Mechanistic insights into PABPC5-mediated regulation of apoptosis in glioma pathophysiology.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- PABPC1 in Cancer: From a Translational Housekeeper to a Stress-Responsive Regulatory Hub.Cancer science · 2026Review
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Authors and funding
10 authors.
Funding
Abstract
Glioma, especially high-grade gliomas like glioblastoma, are aggressive and highly treatment-resistant brain tumors with poor prognosis. Despite advances in therapeutic strategies, the mechanisms driving glioma progression remain inadequately understood, with dysregulated apoptosis playing a central role in malignancy. RNA-binding proteins(RBPs) such as the poly(A)-binding protein family, including PABPC5, have gained attention due to their roles in regulating mRNA stability and translation. PABPC5’s role in glioma pathogenesis remains poorly characterized despite its identification as a key regulator of the mitochondria-associated programmed cell death index (mtPCDI) in low-grade glioma (LGG). This study thoroughly investigated the oncogenic functions of PABPC5. TCGA-GBM analysis revealed significant decreasing trend in PABPC5 expression with increasing glioma grade(G2 vs. G3:P < 0.05; G2vsG4: P < 0.0001;). However, immunohistochemistry and Western blotting demonstrated that PABPC5 protein levels were elevated in Grade 4 tumors compare to Grades 1–3. Notably, expression levels showed no correlation with overall survival (P = 0.92). Lentiviral infection of PABPC5 knockdown in glioblastoma cells (U87/U251) significantly suppressed malignant phenotypes while inducing pro-apoptotic molecular alterations: upregulated BAX and cleaved caspase−3 protein expression, enhanced ROS production, and reduced Bcl−2 and caspase−3 levels. In vivo validation showed that PABPC5 knocdown substantially inhibited subcutaneous tumor growth and increased apoptosis (TUNEL:3.164-fold increase,P < 0.001). Consistent with in vitro findings, immunofluorescence(IF)analysis of tumor tissues confirmed altered Bcl−2/cleaved-caspase−3 expression patterns and mitochondrial ultrastructural changes. This work establishes PABPC5 as a novel biomarker for glioma pathological grading and reveals its functional role in apoptosis regulation. These findings provide a mechanistic foundation for developing therapeutic strategies targeting apoptosis-resistant glioma.
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