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TGF-β-induced expression of IGFBP-3 regulates IGF1R signaling in human osteosarcoma cells.

Abstract：

:Signaling pathways initiated by transforming growth factor-β (TGF-β) and insulin-like growth factors (IGFs) are important in osteosarcoma cell growth. We have investigated a role for endogenous IGF binding protein-3 (IGFBP-3) in mediating cross-talk between TGF-β receptor and type I IGF receptor (IGF1R) signaling pathways in MG-63 osteosarcoma cells. TGF-β1 indirectly activated the Ras/Raf/MAPK pathway and induced the expression of IGFBP-3, an important regulator of IGF1R activity. IGFBP-3 attenuated TGF-β1 activation of ERK1/2 and Akt in MG-63 cells, and inhibited TGF-β1-induced cell cycle progression and proliferation. This effect of IGFBP-3 was blocked by inhibiting IGF1R signaling. TGF-β1 phosphorylated Smad2 on the non-receptor substrate sites (Ser245/250/255). Blocking the TGF-β1-induced expression of IGFBP-3 enhanced pSmad2(Ser245/250/255) and increased its nuclear accumulation. These results suggest an important role for TGF-β1 in osteosarcoma cell growth, with the induction of IGFBP-3 by TGF-β1 serving in a negative-feedback loop to control cell growth by preventing activation of the IGF1R.

journal_name

Mol Cell Endocrinol

journal_title

Molecular and cellular endocrinology

authors

Schedlich LJ,Yenson VM,Baxter RC

doi

10.1016/j.mce.2013.06.033

subject

Has Abstract

pub_date

2013-09-05 00:00:00

pages

56-64

issue

1-2

eissn

0303-7207

issn

1872-8057

pii

S0303-7207(13)00280-3

journal_volume

377

pub_type

杂志文章

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