ArticleBioarchitecture
Dickkopf-3 function in the prostate: implications for epithelial homeostasis and tumor progression.
Article in Bioarchitecture. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- The Multifaceted Role of Human Dickkopf-3 (DKK-3) in Development, Immune Modulation and Cancer.Cells · 2023Review
- Review
- Differential gene methylation patterns in cancerous and non‑cancerous cells.Oncology reports · 2019Article
- Downregulation of C-Terminal Tensin-Like Protein (CTEN) Suppresses Prostate Cell Proliferation and Contributes to Acinar Morphogenesis.International journal of molecular sciences · 2018Article
- Protective effect of stromal Dickkopf-3 in prostate cancer: opposing roles for TGFBI and ECM-1.Oncogene · 2018Article
- CRISPR-Mediated Reactivation of DKK3 Expression Attenuates TGF-β Signaling in Prostate Cancer.Cancers · 2018Article
- Apoptotic Pathways Linked to Endocrine System as Potential Therapeutic Targets for Benign Prostatic Hyperplasia.International journal of molecular sciences · 2016Review
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor suppressor Dickkopf-3 (Dkk-3) is rather a unique molecule. Although it is related to the Dickkopf family of secreted Wnt antagonists, it does not directly inhibit Wnt signaling, and its function and mechanism of action are unknown. Endogenous Dkk-3 was recently found to be required to limit cell proliferation both in the developing mouse prostate and in 3D cultures of human prostate epithelial cells. Dkk-3 was further shown to modulate the response of normal prostate epithelial cells to transforming growth factor-β (TGF-β). These studies are consistent with a model in which Dkk-3 is required by normal cells to prevent the TGF-β switch from tumor suppressor to tumor promoter. Here, we discuss these findings and their potential impact on the development and progression of prostate cancer.
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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.