ArticleOncogene2001
Retinoic acid activates p53 in human embryonal carcinoma through retinoid receptor-dependent stimulation of p53 transactivation function.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 56 citations in OpenAlex.
- Pleiotropic effects of all-trans retinoic acid in attenuating the hallmarks of colorectal cancer- challenges and scope of differentiation therapy.Cancer gene therapy · 2026Review
- Review
- TRAF inhibition drives cancer cell apoptosis and improves retinoic acid sensitivity in multiple cancers models.Discover oncology · 2023Article
- A master of all trades - linking retinoids to different signalling pathways through the multi-purpose receptor STRA6.Cell death discovery · 2021Review
- Article
- Germline genome protection: implications for gamete quality and germ cell tumorigenesis.Andrology · 2019Review
- Epigenetic drugs and their molecular targets in testicular germ cell tumours.Nature reviews. Urology · 2019Review
- Molecular Mechanisms of Cisplatin Chemoresistance and Its Circumventing in Testicular Germ Cell Tumors.Current oncology reports · 2018Review
- p53: key conductor of all anti-acne therapies.Journal of translational medicine · 2017Review
- Refractory testicular germ cell tumors are highly sensitive to the second generation DNA methylation inhibitor guadecitabine.Oncotarget · 2017Article
- Lysine methylation represses p53 activity in teratocarcinoma cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Headway and hurdles in the clinical development of dietary phytochemicals for cancer therapy and prevention: lessons learned from vitamin A derivatives.The AAPS journal · 2014Review
- Cisplatin induces resistance by triggering differentiation of testicular embryonal carcinoma cells.PloS one · 2014Article
- Article
- Potential for Cell-Transplant Therapy with Human Neuronal Precursors to Treat Neuropathic Pain in Models of PNS and CNS Injury: Comparison of hNT2.17 and hNT2.19 Cell Lines.Pain research and treatment · 2012Article
- Serine/threonine kinase 17A is a novel p53 target gene and modulator of cisplatin toxicity and reactive oxygen species in testicular cancer cells.The Journal of biological chemistry · 2011Article
- Effects of ginsenoside Rg2 on the ultraviolet B-induced DNA damage responses in HaCaT cells.Naunyn-Schmiedeberg's archives of pharmacology · 2010Article
- Nucleoside drugs induce cellular differentiation by caspase-dependent degradation of stem cell factors.PloS one · 2010Article
- p53 inactivation by MDM2 and MDMX negative feedback loops in testicular germ cell tumors.Cell cycle (Georgetown, Tex.) · 2010Article
- High DNA methyltransferase 3B expression mediates 5-aza-deoxycytidine hypersensitivity in testicular germ cell tumors.Cancer research · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Although retinoids are known to regulate gene transcription by activating retinoid receptors, the targets of retinoid receptors are largely unknown. This study indicates effective all-trans retinoic acid (RA)-induced differentiation of human embryonal carcinoma cells engages p53. Unexpectedly, RA has been found to activate the transactivation function of p53 in the human embryonal carcinoma cell line, NT2/D1, in a retinoid receptor-dependent manner. A derived RA-resistant line, NT2/D1-R1, is deficient in this activity and is co-resistant to cisplatin. This indicates that RA and cisplatin responses may share a common pathway involving p53 in embryonal carcinomas. RA has no effect on p53 steady-state protein levels in either line. RA enhances endogenous p53 transactivation activity in NT2/D1 but not NT2/D1-R1 cells. In addition, RA induces transactivation activity of a gal4-p53 fusion protein, suggesting that RA activates p53 independent of increasing p53 levels or sequence-specific DNA binding. This activity is absent in retinoic acid receptor gamma (RARgamma)-deficient NT2/D1-R1 cells but can be restored upon co-transfection with specific RARs. Transient transfection of a dominant-negative p53 construct in NT2/D1 cells blocks the RA-mediated transcriptional decline of a differentiation-sensitive reporter plasmid and enhances survival of NT2/D1 cells following cisplatin treatment. Taken together, these findings indicate that RA activates the intrinsic activation function of p53 by a novel mechanism independent of effects on p53 stability or DNA binding and that this activation may be a general mechanism that contributes to RA-mediated G1 arrest.
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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.