ArticleThe Journal of investigative dermatology2022
HDAC1/2 Control Proliferation and Survival in Adult Epidermis and Pre‒Basal Cell Carcinoma through p16 and p53.
Article in The Journal of investigative dermatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
21 citing papers in PubMed, 24 citations in OpenAlex.
- The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026Review
- The impactful role of the HDACs in the regulation of gene expression and as targets for disease therapy.Science advances · 2026Review
- [Potential Mechanisms and Research Advances of HDAC1 in Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026Review
- KRT6A and KRT17 Mark Distinct Stem Cell Populations in the Adult Palpebral Conjunctiva and Meibomian Gland.Cells · 2025Article
- Mechanisms of Okanin against wound healing based on network pharmacology, molecular docking and molecular dynamics simulation.Scientific reports · 2025Article
- Epigenomic regulation of stemness contributes to the low immunogenicity of the most mutated human cancer.Cell reports · 2025Article
- Identification of Meibomian gland stem cell populations and mechanisms of aging.Nature communications · 2025Article
- Histones deacetylases in the epidermis: structure, functions and therapeutic implications.Frontiers in epigenetics and epigenomics · 2025Review
- Identification of Meibomian gland stem cell populations and mechanisms of aging.bioRxiv : the preprint server for biology · 2024Article
- HDAC1/2 and HDAC3 play distinct roles in controlling adult Meibomian gland homeostasis.The ocular surface · 2024Article
- SOX4/HDAC2 Axis Enhances Cell Survivability and Reduces Apoptosis by Activating AKT/MAPK Signaling in Colorectal Cancer.Digestive diseases and sciences · 2024Article
- Inhibition of the CoREST Repressor Complex Promotes Wound Re-Epithelialization through the Regulation of Keratinocyte Migration.The Journal of investigative dermatology · 2024Article
- Transgelin Promotes Glioblastoma Stem Cell Hypoxic Responses and Maintenance Through p53 Acetylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- DOT1L regulates lung developmental epithelial cell fate and adult alveolar stem cell differentiation after acute injury.Stem cell reports · 2023Article
- Korean Red Ginseng Attenuates Particulate Matter-Induced Senescence of Skin Keratinocytes.Antioxidants (Basel, Switzerland) · 2023Article
- The Potential of Senescence as a Target for Developing Anticancer Therapy.International journal of molecular sciences · 2023Review
- HDAC2 as a target for developing anti-cancer drugs.Computational and structural biotechnology journal · 2023Review
- Epigenetic Mechanisms of Epidermal Differentiation.International journal of molecular sciences · 2022Review
- Histone Deacetylases in the Control of Epidermal Homeostasis: From Chromatin Biology toward Therapy.The Journal of investigative dermatology · 2022Article
- Deacetylation of Transcription Factors in Carcinogenesis.International journal of molecular sciences · 2021Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
HDAC inhibitors show therapeutic promise for skin malignancies; however, the roles of specific HDACs in adult epidermal homeostasis and in disease are poorly understood. We find that homozygous epidermal codeletion of Hdac1 and Hdac2 in adult mouse epidermis causes reduced basal cell proliferation, apoptosis, inappropriate differentiation, and eventual loss of Hdac1/2-null keratinocytes. Hdac1/2-deficient epidermis displays elevated acetylated p53 and increased expression of the senescence gene p16. Loss of p53 partially restores basal proliferation, whereas p16 deletion promotes long-term survival of Hdac1/2-null keratinocytes. In activated GLI2-driven pre-basal cell carcinoma, Hdac1/2 deletion dramatically reduces proliferation and increases apoptosis, and knockout of either p53 or p16 partially rescues both proliferation and basal cell viability. Topical application of the HDAC inhibitor romidepsin to the normal epidermis or to GLI2ΔN-driven lesions produces similar defects to those caused by genetic Hdac1/2 deletion, and these are partially rescued by loss of p16. These data reveal essential roles for HDAC1/2 in maintaining proliferation and survival of adult epidermal and basal cell carcinoma progenitors and suggest that the efficacy of therapeutic HDAC1/2 inhibition will depend in part on the mutational status of p53 and p16.
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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.