ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2006
EGF-mediated regulation of IGFBP-3 determines esophageal epithelial cellular response to IGF-I.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- Insulin-like growth factor receptor signaling in physiology and disease.Signal transduction and targeted therapy · 2026Review
- Comparative proteomic analysis of Porphyromonas gingivalis challenged human dental pulp stem cells.Scientific reports · 2025Article
- Modeling Epithelial Homeostasis and Perturbation in Three-Dimensional Human Esophageal Organoids.Biomolecules · 2024Article
- Novel biomarker genes which distinguish between smokers and chronic obstructive pulmonary disease patients with machine learning approach.BMC pulmonary medicine · 2020Article
- 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
- B-Myb Mediates Proliferation and Migration of Non-Small-Cell Lung Cancer via Suppressing IGFBP3.International journal of molecular sciences · 2018Article
- Insulin-like growth factor binding protein-3 is a new predictor of radiosensitivity on esophageal squamous cell carcinoma.Scientific reports · 2015Article
- The p53 family member p73 modulates the proproliferative role of IGFBP3 in short children born small for gestational age.Molecular biology of the cell · 2015Article
- IGFBP3 promotes esophageal cancer growth by suppressing oxidative stress in hypoxic tumor microenvironment.American journal of cancer research · 2014Article
- Everolimus-induced human keratinocytes toxicity is mediated by STAT3 inhibition.Journal of experimental & clinical cancer research : CR · 2013Article
- Nimotuzumab promotes radiosensitivity of EGFR-overexpression esophageal squamous cell carcinoma cells by upregulating IGFBP-3.Journal of translational medicine · 2012Article
- The overexpression of IGFBP-3 is involved in the chemosensitivity of esophageal squamous cell carcinoma cells to nimotuzumab combined with cisplatin.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 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
- Transcriptional profiling of ErbB signalling in mammary luminal epithelial cells--interplay of ErbB and IGF1 signalling through IGFBP3 regulation.BMC cancer · 2010Article
- Insulin-like growth factor-binding protein-3 promotes transforming growth factor-{beta}1-mediated epithelial-to-mesenchymal transition and motility in transformed human esophageal cells.Carcinogenesis · 2010Article
- TLR3-mediated NF-{kappa}B signaling in human esophageal epithelial cells.American journal of physiology. Gastrointestinal and liver physiology · 2009Article
- Insulin-like growth factor and epidermal growth factor treatment: new approaches to protecting steatotic livers against ischemia-reperfusion injury.Endocrinology · 2009Article
- IGFBP-3 regulates esophageal tumor growth through IGF-dependent and independent mechanisms.Cancer biology & therapy · 2007Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
IGF and EGF regulate various physiological and pathological processes. IGF binding protein (IGFBP)-3 regulates cell proliferation in IGF-dependent and -independent fashions. Recently, we identified IGFBP-3 as a novel EGF receptor (EGFR) downstream target molecule in primary and immortalized human esophageal epithelial cells, suggesting an interplay between the EGF and IGF signaling pathways. However, the regulatory mechanisms for IGFBP-3 expression and its functional role in esophageal cell proliferation remain to be elucidated. Herein, we report that IGFBP-3 mRNA and protein were induced upon growth factor deprivation in primary and immortalized human esophageal cells through mechanisms requiring p53-independent de novo mRNA transcription and protein synthesis. This occurred in the face of the activated phosphatidylinositol 3-OH-kinase (PI3K)/mammalian target of rapamycin (mTOR) pathway. Secreted IGFBP-3 neutralized IGFs and prevented IGF-I receptor (IGF-IR) activation. In contrast, EGF suppressed IGFBP-3 mRNA and protein expression through activation of MAPK in an EGFR-tyrosine kinase-dependent manner to restore the cellular response to IGF-I. When stably overexpressed, wild-type IGFBP-3 but not I56G/L80G/L81G (GGG) mutant IGFBP-3, which has a reduced affinity to IGFs, prevented IGF-I from activating IGF-IR and Akt as well as stimulating cell proliferation. However, unlike other cell types where IGFBP-3 exerts antiproliferative effects, neither wild-type nor GGG mutant IGFBP-3 alone affected cell proliferation or EGFR activity. These results indicate that IGF signaling is subject to negative regulation through IGFBP-3 and positive regulation by EGF, the latter of which suppresses IGFBP-3. This provides a platform for understanding the novel cross talk between EGF- and IGF-mediated pathways.
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Registered trials
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