IGF-IR Signaling in Breast Cancer

Clinical and experimental evidence suggest that the insulin-like growth factor receptor (IGF-IR) is involved in breast cancer etiology. For instance, IGF-IR is overexpressed in breast tumors (relative to normal breast epithelium) and high levels of IGF-I (an IGF-IR ligand) correlate with breast canc...

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Bibliographic Details
Main Author: Surmacz, Ewa
Format: Report
Language:English
Subjects:
ADHESION
Anatomy and Physiology
BREAST CANCER
CELLS(BIOLOGY)
CLINICAL MEDICINE
DYNAMICS
EPITHELIUM
ETIOLOGY
GROWTH(PHYSIOLOGY)
IGF IR(INSULIN LIKE GROWTH FACTOR RECEPTOR)
IN VITRO ANALYSIS
INTERACTIONS
MAMMARY GLANDS
Medicine and Medical Research
METASTASIS
NEOPLASMS
RISK
SURVIVAL(PERSONNEL)
WOMEN
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Summary:Clinical and experimental evidence suggest that the insulin-like growth factor receptor (IGF-IR) is involved in breast cancer etiology. For instance, IGF-IR is overexpressed in breast tumors (relative to normal breast epithelium) and high levels of IGF-I (an IGF-IR ligand) correlate with breast cancer risk in premenopausal women. In vitro, IGF-IR regulates the growth and survival of breast cancer cells and plays a role in the development of estrogen-independence. Antiestrogens inhibit IGF-I- dependent growth by interfering with IGF-IR signaling. The mechanisms of this interference are not clear. Here we discuss the evidence that a pure antiestrogen ICI 182,780 specifically blocks breast cancer growth through downregulation of the expression of IRS-i, a major IGF signaling intermediate, Although the role of IGF-IR is breast cancer cell proliferation is clear, its function in growth-unrelated processes, such as cell adhesion, migration and metastasis is less well understood. Here, we report that an IGF-IR signaling substrate SHC, through its dynamic interactions with alpha5beta1integrin (a fibronectin receptor) participates in the regulation of breast cancer cell adhesion and motility.