ArticleFuture science OA2025
Downregulated of CTGF reveals mechanism, remodels immune microenvironment, modulates drug sensitivity in bladder cancer.
Article in Future science OA, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Current Evidence Linking Microplastic Exposure and Reproductive Cancers.Journal of xenobiotics · 2026Review
- Matricellular Proteins in Bladder Cancer: Context-Dependent Roles in Tumor Promotion and Suppression.International journal of molecular sciences · 2026Review
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study aims to investigate the expression profile, molecular mechanisms, and biological functions of Connective Tissue Growth Factor (CTGF) in bladder cancer (BLCA).
methodsFor accurate CTGF mRNA expression assessment, 1728 samples were collected. Additionally, for uncovering potential signaling pathways, differentially co-expressed CTGF genes were employed. For exploring CTGF's effects, its impact on immune microenvironment and drug sensitivity was studied.
resultsCTGF mRNA was significantly underexpressed in BLCA (standardized mean difference [SMD] = -1.06, 95% CI: -1.89-0.23), and this downregulation was confirmed at the protein level (
conclusionsThis study elucidated the low expression of CTGF in BLCA. CTGF may promotes tumor progression by remodeling the immune microenvironment and extracellular matrix. Additionally, its expression is positively correlated with sensitivity to EGFR inhibitors and negatively correlated with resistance to PARP inhibitors.
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