EGF Suppresses the Initiation and Drives the Reversion of TGF-β1-induced Transition in Hepatic Oval Cells Showing the Plasticity of Progenitor Cells

Journal of Cellular Physiology
Ping WangHong You

Abstract

Transforming growth factor-β1 (TGF-β1) induces hepatic progenitors to tumor initiating cells through epithelial-mesenchymal transition (EMT), thus raising an important drawback for stem cell-based therapy. How to block and reverse TGF-β1-induced transition is crucial for progenitors' clinical application and carcinogenic prevention. Rat adult hepatic progenitors, hepatic oval cells, experienced E-cadherin to N-cadherin switch and changed to α-smooth muscle actin (α-SMA) positive cells after TGF-β1 incubation, indicating EMT. When TGF-β1 plus EGF were co-administrated to these cells, EGF dose-dependently suppressed the cadherin switch and α-SMA expression. Interestingly, if EGF was applied to TGF-β1-pretreated cells, the cells that have experienced EMT could return to their epithelial phenotype. Abruption of EGF receptor revealed that EGF exerted its blockage and reversal effects through phosphorylation of ERK1/2 and Akt. These findings suggest an important attribute of EGF on opposing and reversing TGF-β1 effects, indicating the plasticity of hepatic progenitors.

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Citations

Jan 6, 2016·International Journal of Molecular Sciences·Karin Komposch, Maria Sibilia
Feb 18, 2016·Stem Cells International·Guido CarpinoEugenio Gaudio
Jan 26, 2016·The FEBS Journal·Isabel FabregatUNKNOWN IT-LIVER Consortium
May 22, 2020·Frontiers in Cell and Developmental Biology·Francesco BellantiGaetano Serviddio

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