ArticleOncogene2009
Cyclin D1 repressor domain mediates proliferation and survival in prostate cancer.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 24 citations in OpenAlex.
- Cell-cycle targeted cancer therapy: clinical advances, biological gaps, and the emergence of selective CDK4 inhibitors.Journal of hematology & oncology · 2026Review
- Review
- The deregulation of miR-17/CCND1 axis during neuroendocrine transdifferentiation of LNCaP prostate cancer cells.PloS one · 2018Article
- Intensified antineoplastic effect by combining an HDAC-inhibitor, an mTOR-inhibitor and low dosed interferon alpha in prostate cancer cells.Journal of cellular and molecular medicine · 2015Article
- Consequence of the tumor-associated conversion to cyclin D1b.EMBO molecular medicine · 2015Article
- The retinoblastoma tumor suppressor modulates DNA repair and radioresponsiveness.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- Cyclin D2 is a GATA4 cofactor in cardiogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Identification of a cyclin D1 network in prostate cancer that antagonizes epithelial-mesenchymal restraint.Cancer research · 2014Article
- Beyond Breast and Ovarian Cancers: PARP Inhibitors for BRCA Mutation-Associated and BRCA-Like Solid Tumors.Frontiers in oncology · 2014Review
- Dual roles of PARP-1 promote cancer growth and progression.Cancer discovery · 2012Article
- The AR dependent cell cycle: mechanisms and cancer relevance.Molecular and cellular endocrinology · 2012Review
- Galbanic acid decreases androgen receptor abundance and signaling and induces G1 arrest in prostate cancer cells.International journal of cancer · 2012Article
- Cyclin D as a therapeutic target in cancer.Nature reviews. Cancer · 2011Review
- Repression of androgen receptor activity by HEYL, a third member of the Hairy/Enhancer-of-split-related family of Notch effectors.The Journal of biological chemistry · 2011Article
- Cyclin D1 is a selective modifier of androgen-dependent signaling and androgen receptor function.The Journal of biological chemistry · 2011Article
- Starving the addiction: new opportunities for durable suppression of AR signaling in prostate cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Regulation of the androgen receptor (AR) is critical to prostate cancer (PCa) development; therefore, AR is the first line therapeutic target for disseminated tumors. Cell cycle-dependent accumulation of cyclin D1 negatively modulates the transcriptional regulation of AR through discrete, CDK4-independent mechanisms. The transcriptional corepressor function of cyclin D1 resides within a defined motif termed repressor domain (RD), and it was hypothesized that this motif could be utilized as a platform to develop new strategies for blocking AR function. Here, we demonstrate that expression of the RD peptide is sufficient to disrupt AR transcriptional activation of multiple, prostate-specific AR target genes. Importantly, these actions are sufficient to specifically inhibit S-phase progression in AR-positive PCa cells, but not in AR-negative cells or tested AR-positive cells of other lineages. As expected, impaired cell cycle progression resulted in a suppression of cell doubling. Additionally, cell death was observed in AR-positive cells that maintain androgen dependence and in a subset of castrate-resistant PCa cells, dependent on Akt activation status. Lastly, the ability of RD to cooperate with existing hormone therapies was examined, which revealed that RD enhanced the cellular response to an AR antagonist. Together, these data demonstrate that RD is sufficient to disrupt AR-dependent transcriptional and proliferative responses in PCa, and can enhance efficacy of AR antagonists, thus establishing the impetus for development of RD-based mimetics.
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.