Ya Zeng1, Jiahua Yu1, Mina Liu1, Qin Zhang1, Xuwei Cai2. 1. Department of Radiation Oncology, Shanghai Chest Hospital, Shanghai Jiao Tong University, 241 West Huaihai Road, Shanghai, China. 2. Department of Radiation Oncology, Shanghai Chest Hospital, Shanghai Jiao Tong University, 241 West Huaihai Road, Shanghai, China. birdhome2000@163.com.
Abstract
PURPOSE: Vitronectin (VTN), a multifunctional glycoprotein, is involved in various biological and pathological processes. The purpose of this study was to explore the effect of VTN on mesenchymal-epithelial transition (MET) of pulmonary fibroblast cells. METHODS: Lentivirus encoding for VTN-specific shRNA was constructed and infected into the cultured fibroblast WI-38 cells. Real-time PCR and Western blot were applied to examine the expression of VTN in WI-38 cells. MTT assay was used to assess cell proliferation. Western blot was conducted to examine the expression of MET-related and apoptosis-related proteins. RESULTS: The knockdown of VTN significantly inhibited the growth of WI-38 cells compared to the control group. Meanwhile, knockdown of VTN remarkably increased the expression of Bax and Caspase 3 compared with the control group. Furthermore, knockdown of VTN significantly promoted the expression of E-cadherin in comparison to control group. CONCLUSIONS: Knockdown of VTN promoted the expression of apoptosis-related factors, meanwhile, facilitated the MET process of fibroblast cells by regulating the expression of relevant factors. In sum, VTN performed a potential regulator in cell growth and MET of pulmonary fibroblast cells, which can be considered as a potential target for diagnose and therapy of relevant diseases.
PURPOSE: Vitronectin (VTN), a multifunctional glycoprotein, is involved in various biological and pathological processes. The purpose of this study was to explore the effect of VTN on mesenchymal-epithelial transition (MET) of pulmonary fibroblast cells. METHODS: Lentivirus encoding for VTN-specific shRNA was constructed and infected into the cultured fibroblast WI-38 cells. Real-time PCR and Western blot were applied to examine the expression of VTN in WI-38 cells. MTT assay was used to assess cell proliferation. Western blot was conducted to examine the expression of MET-related and apoptosis-related proteins. RESULTS: The knockdown of VTN significantly inhibited the growth of WI-38 cells compared to the control group. Meanwhile, knockdown of VTN remarkably increased the expression of Bax and Caspase 3 compared with the control group. Furthermore, knockdown of VTN significantly promoted the expression of E-cadherin in comparison to control group. CONCLUSIONS: Knockdown of VTN promoted the expression of apoptosis-related factors, meanwhile, facilitated the MET process of fibroblast cells by regulating the expression of relevant factors. In sum, VTN performed a potential regulator in cell growth and MET of pulmonary fibroblast cells, which can be considered as a potential target for diagnose and therapy of relevant diseases.
Authors: Xu-Wei Cai; Kerby Shedden; Xiaoping Ao; Mary Davis; Xiao-Long Fu; Theodore S Lawrence; David M Lubman; Feng-Ming Spring Kong Journal: Int J Radiat Oncol Biol Phys Date: 2010-07-01 Impact factor: 7.038
Authors: Birendra Singh; Anna M Blom; Can Unal; Bo Nilson; Matthias Mörgelin; Kristian Riesbeck Journal: Mol Microbiol Date: 2010-02-19 Impact factor: 3.501