ArticleOncogene2004
Low p21Waf1/Cip1 protein level sensitizes testicular germ cell tumor cells to Fas-mediated apoptosis.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Mechanisms of cisplatin sensitivity and resistance in testicular germ cell tumors and potential therapeutic agents (Review).Experimental and therapeutic medicine · 2025Review
- Breaking the Mold: Epigenetics and Genomics Approaches Addressing Novel Treatments and Chemoresponse in TGCT Patients.International journal of molecular sciences · 2023Review
- Article
- Mechanisms of TP53 Pathway Inactivation in Embryonic and Somatic Cells-Relevance for Understanding (Germ Cell) Tumorigenesis.International journal of molecular sciences · 2021Review
- IGF signalling in germ cells and testicular germ cell tumours: roles and therapeutic approaches.Andrology · 2019Review
- IGF1R signalling in testicular germ cell tumour cells impacts on cell survival and acquired cisplatin resistance.The Journal of pathology · 2018Article
- The chemosensitivity of testicular germ cell tumors.Cellular oncology (Dordrecht, Netherlands) · 2014Review
- Focal adhesion kinase antagonizes doxorubicin cardiotoxicity via p21(Cip1.).Journal of molecular and cellular cardiology · 2014Article
- Pro- and anti-apoptotic effects of p53 in cisplatin-treated human testicular cancer are cell context-dependent.Cell cycle (Georgetown, Tex.) · 2012Article
- p53 hypersensitivity is the predominant mechanism of the unique responsiveness of testicular germ cell tumor (TGCT) cells to cisplatin.PloS one · 2011Article
- Disruption of the MDM2-p53 interaction strongly potentiates p53-dependent apoptosis in cisplatin-resistant human testicular carcinoma cells via the Fas/FasL pathway.Cell death & disease · 2011Article
- Testicular germ cell tumours: predisposition genes and the male germ cell niche.Nature reviews. Cancer · 2011Review
- Cytoplasmic p21 expression levels determine cisplatin resistance in human testicular cancer.The Journal of clinical investigation · 2010Article
- p53 inactivation by MDM2 and MDMX negative feedback loops in testicular germ cell tumors.Cell cycle (Georgetown, Tex.) · 2010Article
- Molecular portrait of cisplatin induced response in human testis cancer cell lines based on gene expression profiles.Molecular cancer · 2007Article
- Testicular Germ Cell Tumors: A Paradigm for the Successful Treatment of Solid Tumor Stem Cells.Current cancer therapy reviews · 2006Article
- Toxicogenomic studies of the rat brain at an early time point following acute sarin exposure.Neurochemical research · 2006Article
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6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the present study, we investigated the relation between p21 expression and the sensitivity of testicular germ cell tumor (TGCT) cells to apoptotic stimuli. Despite similar cisplatin-induced wild-type p53 accumulation, the TGCT cell lines Tera and Scha expressed low p21 protein and mRNA levels in comparison to A2780 ovarian cancer cells. Inhibition of the proteasome complex with MG-132 increased p21 protein levels in TGCT cells but much more in A2780 cells, whereas cisplatin had no additional effect on p21 protein levels. Inhibition of caspase-3 activity in TGCT cells with the broad-spectrum caspase inhibitor zVAD-fmk had no effect on p21 levels and also not upon cisplatin treatment. A similar induction of p53 irradiation, in contrast to cisplatin, substantially increased both p21 mRNA and protein expression in Tera cells. Cisplatin-treated Tera cells expressing low p21 protein levels were Fas-sensitive, while irradiation-induced p21, which was mainly localized in the cytosol, rendered irradiated Tera cells resistant to Fas-induced apoptosis. Sensitivity of irradiated Tera cells to Fas-induced apoptosis was restored by short interfering RNA-specific suppression of p21 expression. These results strongly indicate that the low p21 protein levels are caused by reduced p21 gene transcription and sensitize cisplatin-treated TGCT cells to the Fas death pathway.
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