@Article{096504017X15078984695565,
AUTHOR = {Ting Zhang, Lei Ye, Qizhi He, Jianlong Zhu},
TITLE = {Knockdown of HVEM, a Lymphocyte Regulator Gene,  in Ovarian Cancer Cells Increases Sensitivity to Activated T Cells},
JOURNAL = {Oncology Research},
VOLUME = {25},
YEAR = {2017},
NUMBER = {9},
PAGES = {1665--1665},
URL = {http://www.techscience.com/or/v25n9/56951},
ISSN = {1555-3906},
ABSTRACT = {Ovarian cancer is highly malignant with a gradually increasing incidence and a high mortality rate. Immunosuppression is induced in ovarian cancer, although the mechanism detail is not clear. It has been indicated that 
HVEM (herpesvirus entry mediator) B- and T-lymphocyte attenuator (BTLA) negatively regulates the immune 
responses of T lymphocytes. Here, HVEM mRNA was found to be elevated in ovarian cancer tissue samples 
and primary ovarian cancer cells in comparison with benign tissue samples. We then knocked down HVEM 
expression in an ovarian cancer cell line, OVCAR3, by lentivirus-based small hairpin RNA (shRNA). Cell 
Counting Kit-8 (CCK-8) assay and flow cytometry analysis showed that HVEM-shRNA had no effect on the 
proliferation, early apoptosis, or cell cycle distribution of OVCAR3. We then isolated activated T cells and 
performed coculture experiments in Transwell. Remarkably, HVEM-silenced ovarian cancer cells (primary 
ovarian cancer cells and OVCAR3) increased the number of T cells and the secretion of tumor necrosis factor-a
(TNF-α) and interferon-γ (IFN-γ), while activated T cells promoted the apoptosis of HVEM-silenced ovarian 
cancer cells. The current study partially explains the immune escape mechanism of ovarian cancer cells and 
provides a possible target for immunotherapy.},
DOI = {10.3727/096504017X15078984695565}
}