Oncotarget

Meta-Analysis:

Thymosin-β4 inhibits proliferation and induces apoptosis of hepatic stellate cells through PI3K/AKT pathway

Lili Zhu, Mingliang Cheng _, Yongmei Liu, Yumei Yao, Zixin Zhu, Baofang Zhang, Qiuju Mou and Yiju Cheng

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Oncotarget. 2017; 8:68847-68853. https://doi.org/10.18632/oncotarget.18748

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Abstract

Lili Zhu1,2, Mingliang Cheng1, Yongmei Liu1, Yumei Yao1, Zixin Zhu3, Baofang Zhang1, Qiuju Mou2 and Yiju Cheng1

1Department of Infectious Diseases, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China

2The Affliated Baiyun Hospital of Guizhou Medical University, Guiyang, Guizhou, China

3Guizhou Medical University, Guiyang, Guizhou, China

Correspondence to:

Mingliang Cheng, email: drzuowenshu67@163.com

Keywords: Thymosin-β4, liver fibrosis, hepatic stellate cell, AKT

Received: April 14, 2017     Accepted: May 09, 2017     Published: June 28, 2017

ABSTRACT

Liver fibrosis is a necessary stage for chronic liver diseases, and serious threat to human health. Hepatic fibrosis is a necessary stage for chronic liver diseases. Hepatic stellate cells (HSCs) are the primary cell type responsible for fibrosis. Thymosin beta 4 (Tβ4) has a potential role in the pathogenesis of liver fibrosis and that it is especially associated with the activation of HSCs, however, the underlying mechanisms are not fully elucidated. Herein, we investigated the potential role of Tβ4 in liver fibrosis by describing the effects of Tβ4, and we discuss the possible signaling pathway regulated by Tβ4. The expression of Tβ4 was significantly decreased in human HSC cell line LX-2 and CCl4-treated mouse liver. The depletion of Tβ4 significantly associated with the activation of HSCs via the enhanced expression of α-SMA and vimentin. Tβ4 significantly suppressed the viability and migration of HSCs. Understanding the potential effects and regulatory mechanism of Tβ4 in liver fibrosis might help to provide a novel treatment for patients with liver fibrosis.


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