ArticleJournal of cellular and molecular medicine2025
CAPG Regulates Doxorubicin Resistance in Hepatocellular Carcinoma Cells via TGFB1/Smad/Nrf2 Signalling Pathway.
Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
4 citing papers in PubMed.
- lncRNACancers · 2026Article
- Gambogic acid ameliorates hepatocellular carcinoma by inhibiting oxidative stress via Nrf2-pSmad2C/2L pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Bioinformatic Identification and Preliminary Validation of TP53, TGFB1, and NFE2L2 as Potential Ferroptosis-Related Regulators in Pancreatic Adenocarcinoma.Pharmacogenomics and personalized medicine · 2026Article
- CAPG Regulates Doxorubicin Resistance in Hepatocellular Carcinoma Cells via TGFB1/Smad/Nrf2 Signalling Pathway.Journal of cellular and molecular medicine · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Hepatocellular carcinoma (HCC) is a common and deadly type of liver cancer with limited treatment options and a considerable issue with chemoresistance. This study investigates the role of the cytoskeleton-associated protein G (CAPG) gene in HCC and explores its expression, clinical relevance, as well as the molecular mechanisms on doxorubicin (Dox) resistance. Employing bioinformatics, immunohistochemistry, cell-based assays and animal models, we systematically explored CAPG's function in HCC. Our results demonstrated that CAPG was markedly upregulated in HCC tissues and cell lines compared to normal controls (***p < 0.001). High CAPG expression was associated with poor overall survival (HR = 1.98, p < 0.001) and unfavourable clinicopathological parameters, indicating its potential as a prognostic biomarker. Functional experiments indicated that CAPG knockdown significantly reduced viability and proliferation in Dox-resistant HCC cells (***p < 0.01). Conversely, overexpression promoted resistance. Mechanistically, CAPG appears to modulate ferroptosis via the TGFB1/Smad2/NRF2 signalling pathway, as supported by GSEA analysis and subsequent molecular assays. In vivo, CAPG knockdown in combination with Dox treatment significantly inhibited tumour growth in nude mouse models (***p < 0.01). These findings suggest that CAPG is a pivotal regulator of HCC progression and chemoresistance, offering a promising prognostic biomarker and combinatorial therapeutic target to overcome Dox resistance in clinical settings.
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