Next Article in Journal
Antibacterial Surface Treatment for Orthopaedic Implants
Next Article in Special Issue
Artesunate Induces Apoptosis of Bladder Cancer Cells by miR-16 Regulation of COX-2 Expression
Previous Article in Journal
Theoretical Study of the Transpore Velocity Control of Single-Stranded DNA
Previous Article in Special Issue
Cytotoxic Autophagy in Cancer Therapy
Article Menu
Issue 8 (August) cover image

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2014, 15(8), 13833-13848;

Rapamycin-Induced Apoptosis in HGF-Stimulated Lens Epithelial Cells by AKT/mTOR, ERK and JAK2/STAT3 Pathways

1,†,* , 1
Tianjin Medical University Eye Hospital& Eye Institute, No. 251, Fu Kang Road, Nan Kai District, Tianjin 300384, China
Institute of Innovative Medicine and Food Safety, Jiangsu Berkgen Biopharmaceutical Inc., Ltd., No. 20, Jian Hua Road, Hang Jiang District, Yangzhou 225128, China
These authors contributed equally to this work.
Authors to whom correspondence should be addressed.
Received: 12 May 2014 / Revised: 25 July 2014 / Accepted: 26 July 2014 / Published: 11 August 2014
(This article belongs to the Collection Programmed Cell Death and Apoptosis)
Full-Text   |   PDF [2475 KB, uploaded 12 August 2014]   |  


Hepatocyte growth factor (HGF) induced the proliferation of lens epithelial cells (LECs) and may be a major cause of posterior capsule opacification (PCO), which is the most frequent postoperative complication of cataract surgery. To date, several agents that can block LECs proliferation have been studied, but none have been used in clinic. Recently, accumulating evidence has suggested rapamycin, the inhibitor of mTOR (mammalian target of Rapamycin), was associated with the induction of apoptosis in LECs. The purpose of our study was to investigate the potential effects of rapamycin on HGF-induced LECs and the underlying mechanisms by which rapamycin exerted its actions. Using cell proliferation, cell viability and flow cytometric apoptosis assays, we found that rapamycin potently not only suppressed proliferation but also induced the apoptosis of LECs in a dose-dependent manner under HGF administration. Further investigation of the underlying mechanism using siRNA transfection revealed that rapamycin could promote apoptosis of LECs via inhibiting HGF-induced phosphorylation of AKT/mTOR, ERK and JAK2/STAT3 signaling molecules. Moreover, the forced expression of AKT, ERK and STAT3 could induce a significant suppression of apoptosis in these cells after treatment of rapamycin. Together, these findings suggested that rapamycin-induced apoptosis in HGF-stimulated LECs is accompanied by inhibition of AKT/mTOR, ERK and JAK2/STAT3 pathways, which supports its use to inhibit PCO in preclinical studies and provides theoretical foundation for future possible practice. View Full-Text
Keywords: rapamycin; apoptosis; AKT/mTOR; ERK, JAK2/STAT3 rapamycin; apoptosis; AKT/mTOR; ERK, JAK2/STAT3

Figure 1

This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

Share & Cite This Article

MDPI and ACS Style

Tian, F.; Dong, L.; Zhou, Y.; Shao, Y.; Li, W.; Zhang, H.; Wang, F. Rapamycin-Induced Apoptosis in HGF-Stimulated Lens Epithelial Cells by AKT/mTOR, ERK and JAK2/STAT3 Pathways. Int. J. Mol. Sci. 2014, 15, 13833-13848.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top