Journal
MATRIX BIOLOGY
Volume 56, Issue -, Pages 95-113Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.matbio.2016.06.005
Keywords
Breast cancer; Adhesion; IGF-IR; IGF-I; EGF; E2
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Funding
- European Union (European Social Fund-ESF) [MIS 380222]
- Greek National Funds through the Operational Program Education and Lifelong Learning of the National Strategic Reference Framework (NSRF) Research Funding Program: Thales
- Investing in knowledge society through the European Social Fund [MIS 380222]
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Epidermal growth factor (EGF)/insulin like growth factor-I (IGF-I) and Estradiol (E2) can regulate biological functions of hormone-dependent tumor cells. Fibronectin (FN) is a large glycoprotein abundantly expressed in breast cancer extracellular matrices (ECMs) postulated to be a marker of aggressiveness during cancer pathogenesis. In this study we demonstrate that IGF-I/EGF as well E2 strongly increase the adhesion of the MCF-7 breast cancer cells onto FN. Moreover, IGF-IR is necessary for the IGF-I-/EGF- and E2-induced cell adhesion. Erk1/2 inhibition abolished the IGF-I-/EGF-/E2-induced MCF-7 cell adhesion, suggesting that this regulation of cell adhesion is perpetrated through Erk1/2 downstream signaling. Erk1/2 signaling was shown to modulate IGF-IR status as its' inhibition attenuates both IGF-IR expression and activation. Notably, EGF and E2 enhanced the mRNA as well as protein expression of IGF-IR in MCF-7 cells. Confocal microscopy demonstrated that treatment of MCF-7 cells with IGF-I or EGF induced actin reorganization, which was attenuated with Erk1/2 inhibition. Interestingly, IGF-I treatment induced a co-localization of IGF-IR and FAK, which was evident mostly at the cell membranes of MCF-7 cells. In summary, IGF-IR was shown to be a convergence point for the IGF-/EGF- and E2-dependent MCF-7 cell adhesion onto FN. (C) 2016 Elsevier B.V. All rights reserved.
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