ArticleOncogene2013
C-terminal binding protein-2 regulates response of epithelial ovarian cancer cells to histone deacetylase inhibitors.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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Who cites it
31 citing papers in PubMed, 88 citations in OpenAlex.
- Combined inhibition of NAD synthesis and C-terminal binding protein cooperatively induces cell death and inhibits growth of high grade serous ovarian carcinoma.Scientific reports · 2025Article
- Identification and characterization of a new potent inhibitor targeting CtBP1/BARS in melanoma cells.Journal of experimental & clinical cancer research : CR · 2024Article
- Coordinate transcriptional regulation of ErbB2/3 by C-terminal binding protein 2 signals sensitivity to ErbB2 inhibition in pancreatic adenocarcinoma.Oncogenesis · 2023Article
- Aldolase B attenuates clear cell renal cell carcinoma progression by inhibiting CtBP2.Frontiers of medicine · 2023Article
- The Cynosure of CtBP: Evolution of a Bilaterian Transcriptional Corepressor.Molecular biology and evolution · 2023Article
- Differentially Expressed Bone Marrow microRNAs Are Associated With Soluble HLA-G Bone Marrow Levels in Childhood Leukemia.Frontiers in genetics · 2022Article
- The transrepression and transactivation roles of CtBPs in the pathogenesis of different diseases.Journal of molecular medicine (Berlin, Germany) · 2021Review
- CtBP1/2 differentially regulate genomic stability and DNA repair pathway in high-grade serous ovarian cancer cell.Oncogenesis · 2021Article
- Cryo-EM structure of CtBP2 confirms tetrameric architecture.Structure (London, England : 1993) · 2021Article
- Systematic Profiling of Alternative Splicing Events in Ovarian Cancer.Frontiers in oncology · 2021Article
- Establishment of multifactor predictive models for the occurrence and progression of cervical intraepithelial neoplasia.BMC cancer · 2020Article
- CtBP determines ovarian cancer cell fate through repression of death receptors.Cell death & disease · 2020Article
- Active-Site Tryptophan, the Target of Antineoplastic C-Terminal Binding Protein Inhibitors, Mediates Inhibitor Disruption of CtBP Oligomerization and Transcription Coregulatory Activities.Molecular pharmacology · 2019Article
- An intestinal stem cell niche inOncotarget · 2018Article
- Assembly of human C-terminal binding protein (CtBP) into tetramers.The Journal of biological chemistry · 2018Article
- Transforming activity and therapeutic targeting of C-terminal-binding protein 2 in Apc-mutated neoplasia.Oncogene · 2017Article
- CtBP- an emerging oncogene and novel small molecule drug target: Advances in the understanding of its oncogenic action and identification of therapeutic inhibitors.Cancer biology & therapy · 2017Review
- C-terminal binding protein-2 promotes cell proliferation and migration in breast cancer via suppression of p16INK4A.Oncotarget · 2017Article
- Design, synthesis, and biological evaluation of substrate-competitive inhibitors of C-terminal Binding Protein (CtBP).Bioorganic & medicinal chemistry · 2016Article
- Pinin interacts with C-terminal binding proteins for RNA alternative splicing and epithelial cell identity of human ovarian cancer cells.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ovarian cancer survival rates have stagnated in the last 20 years despite the development of novel chemotherapeutic agents. Modulators of gene expression, such as histone deacetylase (HDAC) inhibitors, are among the new agents being used in clinical trials. Predictors of sensitivity to chemotherapy have remained elusive. In this study, we show that the expression of the transcriptional corepressor C-terminal binding protein-2 (CtBP2) is elevated in human ovarian tumors. Downregulation of CtBP2 expression in ovarian cancer cell lines using short-hairpin RNA strategy suppressed the growth rate and migration of the resultant cancer cells. The knockdown cell lines also showed upregulation of HDAC activity and increased sensitivity to selected HDAC inhibitors. Conversely, forced expression of wild-type CtBP2 in the knockdown cell lines reversed HDAC activity and partially rescued cellular sensitivity to the HDAC inhibitors. We propose that CtBP2 is an ovarian cancer oncogene that regulates gene expression program by modulating HDAC activity. CtBP2 expression may be a surrogate indicator of cellular sensitivity to HDAC inhibitors.
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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.