ArticleOncogene2006
Expression of hTERT immortalises normal human urothelial cells without inactivation of the p16/Rb pathway.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 94 citations in OpenAlex.
- Tissue factor signalling modifies the expression and regulation of G1/S checkpoint regulators: Implications during injury and prolonged inflammation.Molecular medicine reports · 2025Article
- Loss of LPAR6 and CAB39L dysregulates the basal-to-luminal urothelial differentiation program, contributing to bladder carcinogenesis.Cell reports · 2024Article
- The urothelium: a multi-faceted barrier against a harsh environment.Mucosal immunology · 2022Review
- Review
- The effect of antibiotics and photodynamic therapy on extended-spectrum beta-lactamase (ESBL) positive ofSaudi journal of biological sciences · 2021Article
- The Warburg effect as a therapeutic target for bladder cancers and intratumoral heterogeneity in associated molecular targets.Cancer science · 2021Article
- MMP-7 Serum and Tissue Levels Are Associated with Poor Survival in Platinum-Treated Bladder Cancer Patients.Diagnostics (Basel, Switzerland) · 2020Article
- Phosphoproteomic Profiling Identifies Aberrant Activation of Integrin Signaling in Aggressive Non-Type Bladder Carcinoma.Journal of clinical medicine · 2019Article
- ETV5 links the FGFR3 and Hippo signalling pathways in bladder cancer.Scientific reports · 2019Article
- Statins influence epithelial expression of the anti-microbial peptide LL-37/hCAP-18 independently of the mevalonate pathway.Clinical and experimental immunology · 2019Article
- A prospect of cell immortalization combined with matrix microenvironmental optimization strategy for tissue engineering and regeneration.Cell & bioscience · 2019Review
- Implications of TERT promoter mutations and telomerase activity in urothelial carcinogenesis.Nature reviews. Urology · 2018Review
- Circadian coordination of ATP release in the urothelium via connexin43 hemichannels.Scientific reports · 2018Article
- ARID1A-deficiency in urothelial bladder cancer: No predictive biomarker for EZH2-inhibitor treatment response?PloS one · 2018Article
- Ectopic Telomerase Expression Fails to Maintain Chondrogenic Capacity in Three-Dimensional Cultures of Clinically Relevant Cell Types.BioResearch open access · 2018Article
- Proceedings of the 3rd Annual Albert Institute for Bladder Cancer Research Symposium.Bladder cancer (Amsterdam, Netherlands) · 2017Article
- Checkpoint kinase inhibitor AZD7762 strongly sensitises urothelial carcinoma cells to gemcitabine.Journal of experimental & clinical cancer research : CR · 2017Article
- Article
- The New Immortalized Uroepithelial Cell Line HBLAK Contains Defined Genetic Aberrations Typical of Early Stage Urothelial Tumors.Bladder cancer (Amsterdam, Netherlands) · 2016Article
- PIK3CA dependence and sensitivity to therapeutic targeting in urothelial carcinoma.BMC cancer · 2016Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The CDKN2A locus is frequently inactivated in urothelial cell carcinoma (UCC), yet how this alteration contributes to bladder tumorigenesis is not known. Although most UCC express telomerase, inactivation of the p16/Rb pathway is generally required for in vitro immortalisation. This and the involvement of p16 in senescence of normal human urothelial cells (NHUC) suggest that CDKN2A deletion may aid bypass of senescence and allow immortalisation. CDKN2A encodes p16 and p14ARF and therefore inactivation of this locus can disrupt both the Rb and p53 tumour suppressor pathways. Retrovirus-mediated transduction was used to specifically modulate the p16/Rb and/or p53 tumour suppressor pathways in NHUC and to express human telomerase reverse transcriptase (hTERT). Expression of hTERT bypassed Rb and p53 pathway-dependent barriers to proliferation and immortalised NHUC. TERT-NHUC had normal karyotypes, were non-tumorigenic and unexpectedly retained CDKN2A. Thus, the phenotypic significance of inactivation of CDKN2A in UCC may not be solely related to bypass of senescence. Phenotypic assays in human urothelial cells have relied on cell strains derived from invasive tumours or NHUC immortalised by expression of SV40-large T. The production of genetically normal but immortal NHUC lines now provides a valuable platform for experiments to examine the timing and combination of events necessary for UCC tumorigenesis.
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