@Article{096504018X15179694020751,
AUTHOR = {Hai Liu, Xuanxuan Wang, Aihua Huang, Huaping Gao, Yikan Sun, Tingting Jiang, 
Liming Shi, Xianjie Wu, Qinghua Dong, Xiaonan Sun},
TITLE = {Silencing Artemis Enhances Colorectal Cancer Cell  Sensitivity to DNA-Damaging Agents},
JOURNAL = {Oncology Research},
VOLUME = {27},
YEAR = {2019},
NUMBER = {1},
PAGES = {29--38},
URL = {http://www.techscience.com/or/v27n1/48657},
ISSN = {1555-3906},
ABSTRACT = {Artemis is a key protein of NHEJ (nonhomologous end joining), which is the major pathway for the repair 
of IR-induced DSBs in mammalian cells. However, the expression of Artemis in tumors and the influence of 
silencing Artemis on tumor sensitivity to radiation have not been investigated fully. In this study, we investigated how the expression levels of Artemis may affect the treatment outcome of radiotherapy and chemotherapy in colorectal cancer cells. First, we found that the expression of Artemis is strong in some human rectal 
cancer samples, being higher than in adjacent normal tissues using immunohistochemical staining. We then 
knocked down Artemis gene in a human colorectal cancer cell line (RKO) using lentivirus-mediated siRNAs. 
Compared to the control RKO cells, the Artemis knockdown cells showed significantly increased sensitivity 
to bleomycin, etoposide, camptothecin, and IR. Induced by DNA-damaging agents, delayed DNA repair kinetics was found by the -H2AX foci assay, and a significantly increased cell apoptosis occurred in the Artemis 
knockdown RKO cells through apoptosis detection methods and Western blot. We also found that the p53/p21 
signaling pathway may be involved in the apoptosis process. Taken together, our study indicates that manipulating Artemis can enhance colorectal cancer cell sensitivity to DNA-damaging agents. Therefore, Artemis can 
serve as a therapeutic target in rectal cancer therapy.},
DOI = {10.3727/096504018X15179694020751}
}