Over-expression of testis-specific expressed gene 1 attenuates the proliferation and induces apoptosis of GC-1spg cells.
10.1007/s11596-014-1311-3
- Author:
Chao-hui GU
1
;
Feng-yan TIAN
;
Jia-rui PU
;
Li-duan ZHENG
;
Hong MEI
;
Fu-qing ZENG
;
Jin-jian YANG
;
Quan-cheng KAN
;
Qiang-song TONG
Author Information
1. First Affiliated Hospital, Zhengzhou University, Zhengzhou, 450052, China, zgwhgch@qq.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Caspase 8;
biosynthesis;
genetics;
Cell Line;
Cyclin D1;
biosynthesis;
genetics;
G1 Phase;
physiology;
Histones;
genetics;
metabolism;
Ki-67 Antigen;
biosynthesis;
genetics;
Male;
Mice;
Proliferating Cell Nuclear Antigen;
biosynthesis;
genetics;
Resting Phase, Cell Cycle;
physiology;
Spermatogonia;
cytology;
metabolism;
bcl-2-Associated X Protein;
biosynthesis;
genetics
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2014;34(4):535-541
- CountryChina
- Language:English
-
Abstract:
The effects of over-expression of testis-specific expressed gene 1 (TSEG-1) on the viability and apoptosis of cultured spermatogonial GC-1spg cells were investigated, and the immortal spermatogonial cell line GC-1spg (CRL-2053™) was obtained as the cell model in order to explore the function of TSEG-1. We transfected the eukaryotic vector of TSEG-1, named as pEGFP-TSEG-1 into cultured spermatogonial GC-1spg cells. Over-expression of TSEG-1 inhibited the proliferation of GC-1spg cells, and arrested cell cycle slightly at G0/G1 phase. Transfection of TSEG-1 attenuated the transcript levels of Ki-67, PCNA and cyclin D1. In addition, over-expression of TSEG-1 induced early and late apoptosis, and reduced the mitochondrial membrane potential of GC-1spg cells. Moreover, transfection of TSEG-1 significantly enhanced the ratio of Bax/Bcl-2 and transcript levels of caspase 9, and decreased the expression of Fas and caspase 8 in GC-1spg cells. These results indicated over-expression of TSEG-1 suppresses the proliferation and induces the apoptosis of GC-1spg cells, which establishes a basis for further study on the function of TSEG-1.
