ArticleOncogene2001
Inhibitors of histone deacetylase arrest cell cycle and induce apoptosis in cervical carcinoma cells circumventing human papillomavirus oncogene expression.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 111 citations in OpenAlex.
- Review
- The effect of epigenetic reprogramming using MI192 HDAC inhibitor on enhancing the osteogenesis of human adipose-derived stem cells in vitro.Bioscience reports · 2023Article
- Review
- Nuclear oligo hashing improves differential analysis of single-cell RNA-seq.Nature communications · 2022Article
- Epigenetic and Transcriptomic Regulation Landscape in HPV+ Cancers: Biological and Clinical Implications.Frontiers in genetics · 2022Review
- Evaluation of histone deacetylase inhibitor substituted zinc and indium phthalocyanines for chemo- and photodynamic therapy.RSC advances · 2021Article
- Article
- COVID-19 Is a Multi-Organ Aggressor: Epigenetic and Clinical Marks.Frontiers in immunology · 2021Review
- Histone deacetylase 6 inhibition in urothelial cancer as a potential new strategy for cancer treatment.Oncology letters · 2021Article
- Dual targeting of GSK3B and HDACs reduces tumor growth and improves survival in an ovarian cancer mouse model.Gynecologic oncology · 2020Article
- Possible Oncogenic Viruses Associated with Lung Cancer.OncoTargets and therapy · 2020Review
- Increased HDAC Activity and c-MYC Expression Mediate Acquired Resistance to WEE1 Inhibition in Acute Leukemia.Frontiers in oncology · 2020Article
- Oxazole-Bridged Combretastatin A-4 Derivatives with Tethered Hydroxamic Acids: Structure⁻Activity Relations of New Inhibitors of HDAC and/or Tubulin Function.International journal of molecular sciences · 2019Article
- Human papillomavirus and lung cancinogenesis: an overview.Journal of cancer research and clinical oncology · 2016Review
- Extrachromosomal HPV-16 LCR transcriptional activation by HDACi opposed by cellular differentiation and DNA integration.Oncotarget · 2016Article
- Phenylbutyrate-a pan-HDAC inhibitor-suppresses proliferation of glioblastoma LN-229 cell line.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Histone Deacetylase 10 Regulates the Cell Cycle G2/M Phase Transition via a Novel Let-7-HMGA2-Cyclin A2 Pathway.Molecular and cellular biology · 2015Article
- Article
- Cervical Cancer: Development of Targeted Therapies Beyond Molecular Pathogenesis.Current obstetrics and gynecology reports · 2014Article
- Use of reprogrammed cells to identify therapy for respiratory papillomatosis.The New England journal of medicine · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone deacetylase (HDAC) inhibitors sodium butyrate and trichostatin A arrest human papillomavirus (HPV)-positive carcinoma cells in G1 to S transition of the cell cycle, which is paralleled by an up-regulation of the cyclin-dependent kinase inhibitors (CKIs) p21CIP1 and p27KIP1 as well as the complete loss of cdk2 activity. Although HPV expression was hitherto thought to be required to maintain a proliferative phenotype of these cells, cdk2 suppression is achieved even in the presence of ongoing viral transcription. While CKIs normally cannot exert their cdk2-inhibitory function in the presence of the viral oncoprotein E7, co-immunoprecipitation experiments revealed that E7 binding is prevented. Increase of p27KIP1 correlates with down-regulation of p45SKP2, a component of the ubiquitin-protein ligase SCF(SKP2) controlling the half-life of regulatory proteins during the cell cycle. HDAC inhibition also triggered an E7-dependent degradation of pRb, while the levels of E2F remained unaffected. The presence of free intracellular E2F and the concomitant up-regulation of CKIs during G1 arrest results in a 'conflicting growth situation', which finally renders the cells to undergo apoptosis. These data provide novel molecular insights into how the transforming potential of HPV can be bypassed and open new therapeutical perspectives for the treatment of cervical cancer.
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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.