ArticlePloS one2009
Imprinted CDKN1C is a tumor suppressor in rhabdoid tumor and activated by restoration of SMARCB1 and histone deacetylase inhibitors.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 84 citations in OpenAlex.
- Combined inhibition of BETs and HDACs as a potential epigenetics-based therapy for malignant rhabdoid tumor.Cell death & disease · 2026Article
- Enhanced Delivery of Aurora Kinase A Inhibitor Alisertib via Tumor-Targeting Immunoliposome Nanocomplex for Improved Treatment of Cancers Including Atypical Teratoid/Rhabdoid Tumor.International journal of nanomedicine · 2026Article
- Primary diffuse leptomeningeal atypical teratoid/rhabdoid tumours (ATRT) of childhood: a molecularly characterised case report and literature review.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2025Review
- Epigenetic modifications and their roles in pediatric brain tumor formation: emerging insights from chromatin dysregulation.Frontiers in oncology · 2025Review
- STEAP3 promotes colon cancer cell proliferation and migration via regulating histone acetylation.Human genetics · 2024Article
- Targeting Histone 3 Variants Epigenetic Landscape and Inhibitory Immune Checkpoints: An Option for Paediatric Brain Tumours Therapy.Current neuropharmacology · 2024Review
- SMARCB1 Gene Therapy Using a Novel Tumor-Targeted Nanomedicine Enhances Anti-Cancer Efficacy in a Mouse Model of Atypical Teratoid Rhabdoid Tumors.International journal of nanomedicine · 2024Article
- Review on Pediatric Malignant Focal Liver Lesions with Imaging Evaluation: Part II.Diagnostics (Basel, Switzerland) · 2023Review
- Drug-induced loss of imprinting revealed using bioluminescent reporters of Cdkn1c.Scientific reports · 2023Article
- Atypical Teratoid Rhabdoid Tumours Are Susceptible to Panobinostat-Mediated Differentiation Therapy.Cancers · 2021Article
- The FOXM1/RNF26/p57 axis regulates the cell cycle to promote the aggressiveness of bladder cancer.Cell death & disease · 2021Article
- Histone deacetylase inhibitor panobinostat induces antitumor activity in epithelioid sarcoma and rhabdoid tumor by growth factor receptor modulation.BMC cancer · 2021Article
- Current Understanding of Neurofibromatosis Type 1, 2, and Schwannomatosis.International journal of molecular sciences · 2021Review
- Regulation of p27Biomolecules · 2020Review
- Histone Deacetylase Inhibitors in Pediatric Brain Cancers: Biological Activities and Therapeutic Potential.Frontiers in cell and developmental biology · 2020Review
- Epigenetic synthetic lethality approaches in cancer therapy.Clinical epigenetics · 2019Review
- Genetic and Epigenetic Control of CDKN1C Expression: Importance in Cell Commitment and Differentiation, Tissue Homeostasis and Human Diseases.International journal of molecular sciences · 2018Review
- Loss of CDKN1C in a Recurrent Atypical Teratoid/Rhabdoid Tumor.Journal of pediatric hematology/oncology · 2017Article
- Epigenetic modification in chromatin machinery and its deregulation in pediatric brain tumors: Insight into epigenetic therapies.Epigenetics · 2017Review
- Identification of potential therapeutic targets for papillary thyroid carcinoma by bioinformatics analysis.Oncology letters · 2016Article
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
SMARCB1 is deleted in rhabdoid tumor, an aggressive paediatric malignancy affecting the kidney and CNS. We hypothesized that the oncogenic pathway in rhabdoid tumors involved epigenetic silencing of key cell cycle regulators as a consequence of altered chromatin-remodelling, attributable to loss of SMARCB1, and that this hypothesis if proven could provide a biological rationale for testing epigenetic therapies in this disease. We used an inducible expression system to show that the imprinted cell cycle inhibitor CDKN1C is a downstream target for SMARCB1 and is transcriptionally activated by increased histone H3 and H4 acetylation at the promoter. We also show that CDKN1C expression induces cell cycle arrest, CDKN1C knockdown with siRNA is associated with increased proliferation, and is able to compete against the anti-proliferative effect of restored SMARCB1 expression. The histone deacetylase inhibitor (HDACi), Romidepsin, specifically restored CDKN1C expression in rhabdoid tumor cells through promoter histone H3 and H4 acetylation, recapitulating the effect of SMARCB1 on CDKNIC allelic expression, and induced cell cycle arrest in G401 and STM91-01 rhabdoid tumor cell lines. CDKN1C expression was also shown to be generally absent in clinical specimens of rhabdoid tumor, however CDKN1A and CDKN1B expression persisted. Our observations suggest that maintenance of CDKN1C expression plays a critical role in preventing rhabdoid tumor growth. Significantly, we report for the first time, parallels between the molecular pathways of SMARCB1 restoration and Romidepsin treatment, and demonstrate a biological basis for the further exploration of histone deacetylase inhibitors as relevant therapeutic reagents in the treatment of rhabdoid tumor.
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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.