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Silencing Artemis Enhances Colorectal Cancer Cell Sensitivity to DNA-damaging Agents.

Oncology Research 2018 Februrary 10
Artemis is a key protein of NHEJ (non-homologous end-joining), which is the major pathway for the repair of IR-inducedDSBs in mammalian cells. However, it has not been largely investigated about the expression of Artemis in tumor and the influence of silencing Artemis on the tumor's sensitivity to radiation. In this study, we investigated how expression levels of Artemis may affect treatment outcome of radiotherapy and chemotherapy in colorectal cancer cells. Firstly, we found that the expression of Artemis is strong in some human rectal cancer samples, even can be higher than adjacent normal tissues using immunohistochemical staining. We then knocked down Artemis gene in human colorectal cancer cell line (RKO) using lentivirus-mediated siRNAs. As 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 γ-H2AX foci assay and a significantly increased cell apoptosis happened 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 it is applicable to enhance colorectal cancer cell sensitivity to DNA-damaging agents by manipulating Artemis. Artemis can serve as a therapeutic target in rectal cancer therapy.

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