ArticleiScience2026
RBM11 drives malignant progression of bladder cancer by regulating GNPDA1-PKM2 axis.
Article in iScience, 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Integrated Immunotherapy Target Atlas for Ewing Sarcoma.Cancer genomics & proteomicsReview
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study investigated the biological functions and molecular mechanisms of RNA-binding motif protein 11 (RBM11) in bladder cancer (BCa) progression. Integrated bioinformatics analysis of the TCGA database and validation in clinical tissues revealed that RBM11 is significantly upregulated in BCa and positively correlated with advanced tumor stage, poor prognosis, and epithelial-mesenchymal transition (EMT). RBM11 knockdown effectively suppressed migration, invasion, proliferation, and chemoresistance of BCa cells, whereas RBM11 overexpression produced opposite effects. Mechanistically, RBM11 promotes GNPDA1 expression by regulating alternative splicing of GNPDA. Furthermore, GNPDA1 directly interacts with PKM2 and inhibits its ubiquitin-proteasome-mediated degradation, thereby stabilizing PKM2 protein levels, enhancing glycolysis, and promoting malignant progression of BCa. Collectively, these findings indicate that RBM11 drives malignant progression of BCa through the GNPDA1-PKM2 axis, enhancing glucose metabolism reprogramming and EMT process, suggesting that RBM11 may be a potential therapeutic target for BCa.
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Registered trials
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