ArticleMolecular endocrinology (Baltimore, Md.)2009
Enhancing the apoptotic potential of insulin-like growth factor-binding protein-3 in prostate cancer by modulation of CK2 phosphorylation.
Article in Molecular endocrinology (Baltimore, Md.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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
10 citing papers in PubMed, 17 citations in OpenAlex.
- IGFBP3 modulation of tumor pathogenesis and cell signaling pathways (Review).Oncology letters · 2025Review
- Article
- CK2 and the Hallmarks of Cancer.Biomedicines · 2022Review
- Insulin-Like Growth Factor Binding Protein-3 (IGFBP-3): Unraveling the Role in Mediating IGF-Independent Effects Within the Cell.Frontiers in cell and developmental biology · 2020Review
- Article
- The Somatotropic Axis in Human Aging: Framework for the Current State of Knowledge and Future Research.Cell metabolism · 2016Review
- Involvement of the insulin-like growth factor binding proteins in the cancer cell response to DNA damage.Journal of cell communication and signaling · 2015Article
- Pioglitazone restores IGFBP-3 levels through DNA PK in retinal endothelial cells cultured in hyperglycemic conditions.Investigative ophthalmology & visual science · 2014Article
- DNA-PK phosphorylation of IGFBP-3 is required to prevent apoptosis in retinal endothelial cells cultured in high glucose.Investigative ophthalmology & visual science · 2013Article
- Large scale phosphoproteome analysis of LNCaP human prostate cancer cells.Molecular bioSystems · 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
3 authors at 1 institution in 1 country.
Funding
Abstract
IGF-binding protein 3 (IGFBP-3) promotes apoptosis by both IGF-dependent and -independent mechanisms. We have previously reported that phosphorylation of IGFBP-3 (S156) by DNA-dependent protein kinase enhances its nuclear accumulation and is essential for its ability to interact with retinoid X receptor-alpha and induce apoptosis in cultured prostate cancer cells. Using specific chemical inhibitors and small interfering RNA, we demonstrate that preventing casein kinase 2 (CK2) activation enhanced the apoptotic potential of IGFBP-3. We mapped potential CK2 phosphosphorylation sites in IGFBP-3 to S167 and S175 and identified that wild-type IGFBP-3- and IGFBP-3-S175A-induced apoptosis to a comparable extent. In contrast, IGFBP-3-S167A was far more potently apoptosis inducing due to inability to undergo CK2 phosphorylation. Pretreatment of 22RV1 cells with IGFBP-3 small interfering RNA also limits the ability of high doses of CK2 inhibitor to induce apoptosis. These effects can be reversed by the addition of exogenous IGFBP-3 protein, suggesting reciprocal regulation of cell survival and apoptosis by IGFBP-3 and CK2. These studies reveal multisite phosphorylation of IGFBP-3 that both positively and negatively regulate its apoptotic potential. Understanding such intrinsic regulation of IGFBP-3 action may enhance the development of potential cancer therapies.
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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.