Year: 2011
Type: article
Abstract: INTRODUCTION Transforming growth factor- (TGFβ) acts as a potent tumor suppressor and tumor promoter in a context-dependent manner [1]. Tumor suppressive functions include inhibition of cell proliferation, induction of apoptosis and regulation of autophagy. As tumors develop they switch their response to TGFβ and utilize this factor as a potent promoter of cell motility, invasion, metastasis and tumor stem cell maintenance. It has been widely proved that misregulation of TGFβ, i .e. TGFβ over-expression, TGFβ receptor or Smad2/4 loss or mutation, can result in tumor development [2]. Epidermal Growth Factor (EGF) is another potent regulator of cell functions, with predominantly pro-mitogenic role in tumorigenesis [3]. EGF promotes also cell survival, angiogenesis and differentiation. Deregulation of human epidermal growth factor receptor (ErbB/HER) pathways by over-expression or constitutive activation can promote tumorigenesis, including angiogenesis and metastasis and is associated with poor prognosis in many human malignancies [4]. TGF and EGF initiate signaling events via acting on different receptors. However, recent reports indicate that many of the components in their intracellular signaling pathways may be targeted by both growth factors. Understanding the molecular mechanisms of how TGFβ and EGF signaling interact at different stages of cancer is important for development of novel therapeutics. In this report, we focus on TGF and EGF signaling, with emphasis on the cross-talk between their regulatory pathways.
Source: PubMed
Authors: M Jia, S Souchelnytstkyi
Institution: Karolinska Institutet
Language: English
Topic: TGF-β signaling in diseases
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W2427463100