ArticleNaunyn-Schmiedeberg's archives of pharmacology2024
PDE3B regulates KRT6B and increases the sensitivity of bladder cancer cells to copper ionophores.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Clinacanthus nutans (Burm.f.) Lindau facilitates cuproptosis and ameliorates colon cancer progression by inhibiting PDE3B-mediated Apelin pathway.Discover oncology · 2025Article
- Tanshinone IIA promotes METTL3/METTL14-mediated FDX1 m6A modification to induce cuproptosis in bladder cancer.Toxicology research · 2025Article
- Identification of prognostic and therapeutic biomarkers associated with macrophage and lipid metabolism in pancreatic cancer.Scientific reports · 2025Article
- A p-n heterojunction sonosensitizer for improved sono-immunotherapy via induction of multimodal cell death mechanisms.Theranostics · 2025Article
- Causal effect of interstitial lung disease on lung cancer risk in never-smokers and prognostic insights from Mendelian randomization and transcriptome analysis.American journal of cancer research · 2025Article
- Cuproptosis-related genes and agents: implications in tumor drug resistance and future perspectives.Frontiers in pharmacology · 2025Review
- Copper homeostasis and copper-induced cell death in tumor immunity: implications for therapeutic strategies in cancer immunotherapy.Biomarker research · 2024Review
- Preparation of kakkatin derivatives and their anti-tumor activity.World journal of clinical oncology · 2024Article
- Novel insights into cuproptosis inducers and inhibitors.Frontiers in molecular biosciences · 2024Review
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
Cuproptosis is a new Cu-dependent programmed cell death manner that has shown regulatory functions in many tumor types, however, its mechanism in bladder cancer remains unclear. Here, we reveal that Phosphodiesterase 3B (PDE3B), a cuproptosis-associated gene, could reduce the invasion and migration of bladder cancer. PDE3B is downregulated in bladder cancer tissues, which is correlated with better prognosis. Conversely, overexpression of PDE3B in bladder cancer cell could significantly resist invasion and migration, which is consistent with the TCGA database results. Future study demonstrate the anti-cancer effect of PDE3B is mediated by Keratin 6B (KRT6B) which leads to the keratinization. Therefore, PDE3B can reduce KRT6B expression and inhibit the invasion and migration of bladder cancer. Meanwhile, increased expression of PDE3B was able to enhance the sensitivity of Cuproptosis drug thiram. This study show that PDE3B/KRT6B is a potential cancer therapeutic target and PDE3B activation is able to increase the sensitivity of bladder cancer cells to copper ionophores.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.