ArticleCancers2019
Hyper-Activation of STAT3 Sustains Progression of Non-Papillary Basal-Type Bladder Cancer via FOSL1 Regulome.
Article in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 47 citations in OpenAlex.
- DSG3 promotes bladder cancer growth and metastasis via AKT/GSK3β/β-catenin pathway.Journal of translational medicine · 2025Article
- Molecular profiling of bladder cancer xenografts defines relevant molecular subtypes and provides a resource for biomarker discovery.Translational oncology · 2025Article
- From dysbiosis to precision therapy: decoding the gut-bladder axis in bladder carcinogenesis.Frontiers in oncology · 2025Review
- Pan-cancer analysis of STAT3 indicates its potential prognostic value and correlation with immune cell infiltration in prostate cancer.Discover oncology · 2024Article
- Stat3 Inhibitors TTI-101 and SH5-07 Suppress Bladder Cancer Cell Survival in 3D Tumor Models.Cells · 2024Article
- SARS-CoV-2 Protein Nsp9 Is Involved in Viral Evasion through Interactions with Innate Immune Pathways.ACS omega · 2024Article
- Digital spatial profiling of the microenvironment of muscle invasive bladder cancer.Communications biology · 2024Article
- A novel anoikis-related gene signature identifies LYPD1 as a novel therapy target for bladder cancer.Scientific reports · 2024Article
- The Urinary Microbiome in Health and Disease: Relevance for Bladder Cancer.International journal of molecular sciences · 2024Review
- CENPW knockdown inhibits progression of bladder cancer through inducing cell cycle arrest and apoptosis.Journal of Cancer · 2024Article
- The combination treatment of RC48 and STAT3 inhibitor acts as a promising therapeutic strategy for basal bladder cancer.Frontiers in immunology · 2024Article
- Inhibition of microRNA-34c reduces detrusor ROCK2 expression and urinary bladder inflammation in experimental cystitis.Life sciences · 2024Article
- The role of microbiota in tumorigenesis, progression and treatment of bladder cancer.Microbiome research reports · 2024Review
- The urothelial gene regulatory network: understanding biology to improve bladder cancer management.Oncogene · 2024Review
- Influence of Long Non-Coding RNA in the Regulation of Cancer Stem Cell Signaling Pathways.Cells · 2022Review
- Pharmacokinetics and Biological Activity of Cucurbitacins.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Review
- The Urinary Microbiome: Role in Bladder Cancer and Treatment.Diagnostics (Basel, Switzerland) · 2022Review
- Role of Nrf2, STAT3, and Src as Molecular Targets for Cancer Chemoprevention.Pharmaceutics · 2022Review
- Cancer and Covid-19: Collectively catastrophic.Cytokine & growth factor reviews · 2022Review
Corrections and comments
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Authors and funding
18 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Urothelial bladder cancer (UBC) are classified into luminal and basal subtypes showing distinct molecular features and clinical behaviour. Recent in silico data have proposed the activation on the Signal Transducer and Activator of Transcription 3 (STAT3) as relevant transcription factor in UBC. To answer this question, we have combined the retrospective analysis of clinical samples, functional assays on cell lines, interrogation of public UBC datasets and a murine model of basal-type UBC. Immunohistochemistry on a retrospective UBC cohort uncovered that STAT3 Y705 phosphorylation (pSTAT3) is significantly increased in infiltrating basal-type UBC compared to luminal UBC. In vitro, STAT3 silencing in UBC cell lines significantly reduced tumor cell viability and invasion. Gene expression profile of UBC cell lines combined with the analysis of the Cancer Genome Atlas (TCGA) and GSE32894 UBC datasets showed that increased expression of a set of STAT3 targets predicts basal-type, propensity to local progression and worse prognosis. MYC and FOSL1 represent relevant STAT3 downstream targets, as validated by their co-localization in pSTAT3+ UBC cancer cells. These findings were largely reproduced in the BBN-induced murine model of basal-type UBC. Of note, FOSL1 protein resulted strongly expressed in the non-papillary UBC pathway and FOSL1-regulated transcripts were significantly enriched in the transition from NMIBC to MIBC, as indicated by the interrogation of the GSE32894 dataset. The blockade of the STAT3 pathway might represent a novel treatment option for these neoplasms. Monitoring pSTAT3 and the downstream targets, particularly FOSL1, could provide meaningful levels of UBC stratification.
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