ArticleMolecular cancer research : MCR2014
DNA damage-binding complex recruits HDAC1 to repress Bcl-2 transcription in human ovarian cancer cells.
Article in Molecular cancer research : MCR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- iModEst: disentangling -omic impacts on gene expression variation across genes and tissues.NAR genomics and bioinformatics · 2025Article
- Epigenetic Modulation of Estrogen Receptor Signaling in Ovarian Cancer.International journal of molecular sciences · 2024Review
- Identification of protein biomarkers for prediction of response to platinum-based treatment regimens in patients with non-small cell lung cancer.Molecular oncology · 2024Article
- A protein with broad functions: damage-specific DNA-binding protein 2.Molecular biology reports · 2022Review
- Histone deacetylation regulates nucleotide excision repair through an interaction with the XPC protein.iScience · 2022Article
- The E2F1 transcription factor and RB tumor suppressor moonlight as DNA repair factors.Cell cycle (Georgetown, Tex.) · 2020Review
- Carotenoids in Cancer Apoptosis-The RoadCancers · 2020Review
- Article
- Depletion of DNA damage binding protein 2 sensitizes triple-negative breast cancer cells to poly ADP-ribose polymerase inhibition by destabilizing Rad51.Cancer science · 2019Article
- Emerging Roles of DDB2 in Cancer.International journal of molecular sciences · 2019Review
- Inhibition of miR-328-3p Impairs Cancer Stem Cell Function and Prevents Metastasis in Ovarian Cancer.Cancer research · 2019Article
- DDB2 regulates Epithelial-to-Mesenchymal Transition (EMT) in Oral/Head and Neck Squamous Cell Carcinoma.Oncotarget · 2018Article
- DDB2 represses ovarian cancer cell dedifferentiation by suppressing ALDH1A1.Cell death & disease · 2018Article
- UV radiation-induced SUMOylation of DDB2 regulates nucleotide excision repair.Carcinogenesis · 2017Article
- DDB2 increases radioresistance of NSCLC cells by enhancing DNA damage responses.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- DDB2 modulates TGF-β signal transduction in human ovarian cancer cells by downregulating NEDD4L.Nucleic acids research · 2015Article
- Damaged DNA-binding protein down-regulates epigenetic mark H3K56Ac through histone deacetylase 1 and 2.Mutation research · 2015Article
- DDB2 suppresses tumorigenicity by limiting the cancer stem cell population in ovarian cancer.Molecular cancer research : MCR · 2014Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledElevated expression of the antiapoptotic factor Bcl-2 is believed to be one of the contributing factors to an increased relapse rate associated with multiple cisplatin-resistant cancers. DNA damage-binding protein complex subunit 2 (DDB2) has recently been revealed to play an important role in sensitizing human ovarian cancer cells to cisplatin-induced apoptosis through the downregulation of Bcl-2, but the underlying molecular mechanism remains poorly defined. Here, it is report that DDB2 functions as a transcriptional repressor for Bcl-2 in combination with DDB1. Quantitative ChIP and EMSA analysis revealed that DDB2 binds to a specific cis-acting element at the 5'-end of Bcl-2 P1 promoter. Overexpression of DDB2 resulted in marked losses of histone H3K9,14 acetylation along the Bcl-2 promoter and enhancer regions, concomitant with a local enrichment of HDAC1 to the Bcl-2 P1 core promoter in ovarian cancer cells. Coimmunoprecipitation and in vitro binding analyses identified a physical interaction between DDB1 and HDAC1, whereas downregulation of HDAC1 significantly enhanced Bcl-2 promoter activity. Finally, in comparison with wild-type DDB2, mutated DDB2, which is unable to repress Bcl-2 transcription, mediates a compromised apoptosis upon cisplatin treatment. Taken together, these data support a model wherein DDB1 and DDB2 cooperate to repress Bcl-2 transcription. DDB2 recognizes and binds to the Bcl-2 P1 promoter, and HDAC1 is recruited through the DDB1 subunit associated with DDB2 to deacetylate histone H3K9,14 across Bcl-2 regulatory regions, resulting in suppressed Bcl-2 transcription. IMPLICATIONS: Increasing the expression of DDB complex may provide a molecular strategy for cancer therapy.
Indexed as
Identifiers
What OpenQuestion holds
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.