Pathologic Signaling and Disease Implications of Insulin-like Growth Factor Binding Proteins in Cancer, Cardiovascular Disease, and Fibrosis
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Updated: Jan 11, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
Zachary R Sechrist1,2,3, Jaeden S Cortés2,3, Nidhi R Patel2,3
1Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA.
Abstract:
The insulin-like growth factor binding protein (IGFBP) family consists of seven members, which are known for their roles in regulating canonical insulin-like growth factor (IGF) signaling and, more recently, a variety of non-canonical signaling pathways. This review will explore shared pathologic mechanisms amongst the IGFBP family members in diseases like cancer and fibrosis which reveal the unique and redundant properties of this critical family of proteins and provides unique insight into how their regulation is not only relevant to cell metabolism, but also plays an emerging role in diverse processes including immunity, TGF-β signaling, hypoxia and angiogenesis, and senescence. Moreover, these molecules have shown promise both as biomarkers and therapeutics, and a deeper understanding of this system is needed to appreciate how leveraging their regulation may be able to ameliorate diverse organ pathologies.
Insights
The insulin-like growth factor binding protein (IGFBP) family regulates cell signaling and metabolism. Understanding IGFBP roles in diseases like cancer and fibrosis offers therapeutic and biomarker potential.
Area of Science:
- Biochemistry
- Molecular Biology
- Cell Biology
Background:
- The insulin-like growth factor binding protein (IGFBP) family comprises seven members.
- These proteins regulate canonical insulin-like growth factor (IGF) signaling.
- Emerging evidence highlights their roles in non-canonical signaling pathways.
Purpose of the Study:
- To review shared pathologic mechanisms of IGFBP family members in diseases.
- To explore unique and redundant properties of IGFBPs.
- To provide insight into IGFBP regulation in diverse cellular processes.
Main Methods:
- Literature review of IGFBP family functions.
- Analysis of IGFBP roles in cancer and fibrosis.
- Exploration of IGFBP involvement in immunity, TGF-β signaling, hypoxia, angiogenesis, and senescence.
Main Results:
- IGFBP family members share pathologic mechanisms in diseases.
- IGFBP regulation impacts cell metabolism, immunity, and senescence.
- IGFBP functions extend to TGF-β signaling, hypoxia, and angiogenesis.
Conclusions:
- Understanding IGFBP family complexity is crucial for disease pathology.
- IGFBP regulation offers potential as biomarkers and therapeutics.
- Leveraging IGFBP regulation may ameliorate diverse organ pathologies.
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