Downregulation of cellular prion protein inhibited the proliferation and invasion and induced apoptosis of Marek's disease virus-transformed avian T cells.
10.4142/jvs.2016.17.2.171
- Author:
Xuerui WAN
1
;
Runxia YANG
;
Guilin LIU
;
Manling ZHU
;
Tianliang ZHANG
;
Lei LIU
;
Run WU
Author Information
1. Department of Preventive Veterinary, College of Veterinary Medicine, Gansu Agricultural University, Lanzhou 730070, China. wurun@gsau.edu.cn
- Publication Type:Original Article
- Keywords:
Marek's disease virus-transformed avian T cells;
apoptosis;
chicken prion protein;
invasion;
short interfering RNA
- MeSH:
Animals;
Apoptosis*;
Carcinogenesis;
Cell Cycle;
Cell Proliferation;
Chickens;
Down-Regulation*;
Eukaryotic Cells;
Mammals;
Marek Disease*;
RNA, Small Interfering;
T-Lymphocytes*
- From:Journal of Veterinary Science
2016;17(2):171-178
- CountryRepublic of Korea
- Language:English
-
Abstract:
Cellular prion protein (PrP(C)) is ubiquitously expressed in the cytomembrane of a considerable number of eukaryotic cells. Although several studies have investigated the functions of PrP(C) in cell proliferation, cell apoptosis, and tumorigenesis of mammals, the correlated functions of chicken PrP(C) (chPrP(C)) remain unknown. In this study, stable chPrP(C)-downregulated Marek's disease (MD) virus-transformed avian T cells (MSB1-SiRNA-3) were established by introducing short interfering RNA (SiRNA) targeting chicken prion protein genes. We found that downregulation of chPrP(C) inhibits proliferation, invasion, and migration, and induces G1 cell cycle phase arrest and apoptosis of MSB1-SiRNA-3 cells compared with Marek's disease virus-transformed avian T cells (MSB1) and negative control cells. To the best of our knowledge, the present study provides the first evidence supporting the positive correlation between the expression level of chPrP(C) and the proliferation, migration, and invasion ability of MSB1 cells, but appears to protect MSB1 cells from apoptosis, which suggests it functions in the formation and development of MD tumors. This evidence may contribute to future research into the specific molecular mechanisms of chPrP(C) in the formation and development of MD tumors.
