ArticleThe Journal of biological chemistry2010
IGFBP-3 can either inhibit or enhance EGF-mediated growth of breast epithelial cells dependent upon the presence of fibronectin.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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Who cites it
20 citing papers in PubMed, 39 citations in OpenAlex.
- Modelling the Tumor Microenvironment: Recapitulating Nano- and Micro-Scale Properties that Regulate Tumor Progression.Frontiers in cell and developmental biology · 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
- Fibrillin microfibrils and elastic fibre proteins: Functional interactions and extracellular regulation of growth factors.Seminars in cell & developmental biology · 2019Review
- Insulin-like growth factor binding protein-3 links obesity and breast cancer progression.Oncotarget · 2016Article
- Deregulation of IGF-binding proteins -2 and -5 contributes to the development of endocrine resistant breast cancer in vitro.Oncotarget · 2016Article
- Impact of IGF-1, IGF-1R, and IGFBP-3 promoter methylation on the risk and prognosis of esophageal carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Insulin-like growth factor binding protein-3 is a new predictor of radiosensitivity on esophageal squamous cell carcinoma.Scientific reports · 2015Article
- Estrogen Receptor-β and the Insulin-Like Growth Factor Axis as Potential Therapeutic Targets for Triple-Negative Breast Cancer.Critical reviews in oncogenesis · 2015Review
- Epithelial-to-mesenchymal transition in breast cancer: a role for insulin-like growth factor I and insulin-like growth factor-binding protein 3?Breast cancer (Dove Medical Press) · 2015Review
- β-D-glucan inhibits endocrine-resistant breast cancer cell proliferation and alters gene expression.International journal of oncology · 2014Article
- The role of insulin-like growth factor binding protein-3 in the breast cancer cell response to DNA-damaging agents.Oncogene · 2014Article
- Differential Effects of Insulin-Like Growth Factor Binding Protein-6 (IGFBP-6) on Migration of Two Ovarian Cancer Cell Lines.Frontiers in endocrinology · 2014Article
- Genetic polymorphisms in IGF-I and IGFBP-3 are associated with prostate cancer in the Chinese population.PloS one · 2014Article
- Article
- Insulin-like growth factor binding protein-3 (IGFBP-3): Novel ligands mediate unexpected functions.Journal of cell communication and signaling · 2013Article
- IGFBP-3 binds GRP78, stimulates autophagy and promotes the survival of breast cancer cells exposed to adverse microenvironments.Oncogene · 2013Article
- Histone deacetylase inhibitors enhance the apoptotic activity of insulin-like growth factor binding protein-3 by blocking PKC-induced IGFBP-3 degradation.International journal of cancer · 2012Article
- Protein expression changes during human triple negative breast cancer cell line progression to lymph node metastasis in a xenografted model in nude mice.Cancer biology & therapy · 2012Article
- Hypoxia induces IGFBP3 in esophageal squamous cancer cells through HIF-1α-mediated mRNA transcription and continuous protein synthesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012Article
- Intrinsic, Pro-Apoptotic Effects of IGFBP-3 on Breast Cancer Cells are Reversible: Involvement of PKA, Rho, and Ceramide.Frontiers in endocrinology · 2011Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Progression of breast cancer is associated with remodeling of the extracellular matrix, often involving a switch from estrogen dependence to a dependence on EGF receptor (EGFR)/HER-2 and is accompanied by increased expression of the main binding protein for insulin-like growth factors (IGFBP-3). We have examined the effects of IGFBP-3 on EGF responses of breast epithelial cells in the context of changes in the extracellular matrix. On plastic and laminin with MCF-10A normal breast epithelial cells, EGF and IGFBP-3 each increased cell growth and together produced a synergistic response, whereas with T47D breast cancer cells IGFBP-3 alone had no effect, but the ability of EGF to increase cell proliferation was markedly inhibited in the presence of IGFBP-3. In contrast on fibronectin with MCF-10A cells, IGFBP-3 alone inhibited cell growth and blocked EGF-induced proliferation. With the cancer cells, IGFBP-3 alone had no effect but enhanced the EGF-induced increase in cell growth. The insulin-like growth factor-independent effects of IGFBP-3 alone on cell proliferation were completely abrogated in the presence of an EGFR, tyrosine kinase inhibitor, Iressa. Although IGFBP-3 did not affect EGFR phosphorylation [Tyr(1068)], it was found to modulate receptor internalization and was associated with activation of Rho and subsequent changes in MAPK phosphorylation. The levels of fibronectin and IGFBP-3 within breast tumors may determine their dependence on EGFR and their response to therapies targeting this receptor.
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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.