ArticleCancer research2011
IGFBP-3 is a metastasis suppression gene in prostate cancer.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 4 of them syntheses that pooled it.
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
59 citing papers in PubMed, 4 syntheses or guidelines pooled it, 92 citations in OpenAlex.
- Association between the IGFBP-3 rs2854744 polymorphism and cancer risk: a meta-analysis.BMC medical genomics · 2026Pooled it
- Pooled it
- Does milk intake promote prostate cancer initiation or progression via effects on insulin-like growth factors (IGFs)? A systematic review and meta-analysis.Cancer causes & control : CCC · 2017Pooled it
- Pooled it
- Prognostic significance of psoas muscle index at diagnosis in cervical cancer progression.Journal of gynecologic oncology · 2026Article
- Synergistic cytotoxicity of recombinant IGFBP-3 and cisplatin in HPV18-positive HeLa cellsResearch in pharmaceutical sciences · 2026Article
- Mechanistic insights and clinical implications of RNA-binding proteins in prostate cancer.Discover oncology · 2026Review
- Proteome-wide association study of prostate cancer risk across populations.Nature communications · 2025Article
- In Vitro and In Silico Evaluation of the Potential Anti-Prostate Cancer Activity ofInternational journal of molecular sciences · 2025Article
- Interactions between androgen and IGF1 axes in prostate tumorigenesis.Nature reviews. Urology · 2025Review
- DNA methylation markers for risk of metastasis in a cohort of men with localized prostate cancer.Epigenetics · 2024Article
- DRMref: comprehensive reference map of drug resistance mechanisms in human cancer.Nucleic acids research · 2024Article
- Cell cycle control by the insulin-like growth factor signal: at the crossroad between cell growth and mitotic regulation.Cell cycle (Georgetown, Tex.) · 2023Review
- Insulin-like growth factor role in determining the anti-cancer effect of metformin: RCT in prostate cancer patients.Endocrine connections · 2022Article
- Expression of Recombinant Insulin-Like Growth Factor-Binding Protein-3 Receptor in Mammalian Cell Line and Prokaryotic (Advanced biomedical research · 2022Article
- Phenotypic characterization of two novel cell line models of castration-resistant prostate cancer.The Prostate · 2021Article
- Evaluation of circulating IGF-I and IGFBP-3 as biomarkers for tumors in dogs.Journal of veterinary science · 2021Article
- The tumor suppressor miR-642a-5p targets Wilms Tumor 1 gene and cell-cycle progression in prostate cancer.Scientific reports · 2021Article
- Insulin-like growth factor binding protein 3 promotes radiosensitivity of oral squamous cell carcinoma cells via positive feedback on NF-κB/IL-6/ROS signaling.Journal of experimental & clinical cancer research : CR · 2021Article
- Article
Corrections and comments
- Commented on by
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
The insulin-like growth factor binding protein IGFBP-3 is a proapoptotic and antiangiogenic protein in prostate cancer (CaP). Epidemiologic studies suggest that low IGFBP-3 is associated with greater risk of aggressive, metastatic prostate cancers, but in vivo functional data are lacking. Here we show that mice that are genetically deficient in IGFBP-3 exhibit weaker growth of primary prostate tumors but higher incidence of metastatic disease. Prostates in IGFBP-3 knockout mice (IGFBP-3KO mice) failed to undergo apoptosis after castration. Spontaneous prostate tumors did not develop in IGFBP-3KO mice, but splenic lymphomas occurred in 23% of female IGFBP-3KO mice by 80 weeks of age. To assess the effects of IGFBP-3 deficiency on prostate cancer development, we crossed IGFBP-3KO mice with a c-Myc-driven model of CaP that develops slow-growing, nonmetastatic tumors. By 24 weeks of age, well-differentiated prostate cancers were observed in all mice regardless of IGFBP-3 status. However, by 80 weeks of age IGFBP-3KO mice tended to exhibit larger prostate tumors than control mice. More strikingly, lung metastases were observed at this time in 55% of the IGFBP-3KO mice but none in the control animals. Cell lines established from IGFBP-3KO:Myc tumors displayed more aggressive phenotypes in proliferation, invasion, and colony formation assays, relative to control Myc tumor cell lines. In addition, Myc:IGFBP-3KO cells exhibited evidence of epithelial-mesenchymal transition. Our findings established a function for IGFBP-3 in suppressing metastasis in prostate cancer, and they also offered the first reported transgenic model of spontaneous metastatic prostate cancer for studies of this advanced stage of disease.
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.