WY, ZL, WZ, JZ and AL collected the examples, and participated in the collection and analysis of data. restored. In the present, down rules of RAD51 by shRNA and imatinib sensitized Jurkat cells to etoposide by reducing the activity of homologous recombination (HR). We found that the suppression of RAD51 by shRNA inhibited tumor cells proliferation and enhanced apoptosis of Jurkat cells after etoposide treatment. Importantly, downregulation of RAD51 by imatinib obviously improved the apoptosis of Jurkat cell after etoposide treatment. These results shown that RAD51 may be of great value to like a novel target for the medical treatment of adult T-cell leukemia-lymphoma (ATL), and it may improve the survival of leukemia individuals. studies of CPUY074020 RAD51 activity. As shRNA is not currently applied in medical treatment, inhibition of RAD51 with imatinib was also used in the current study (24). Imatinib is the first-line therapy for chronic myelocytic leukemia. It has been reported that imatinib treatment reduces the manifestation of RAD51 and is closely associated with reduced HR in tumor cell lines with CPUY074020 different p53 claims (18). Treatment of tumor cells with imatinib enhances level of sensitivity (24), but this effect does not happen in normal fibroblasts. In irradiated tumors, mitomycin, gemcitabine combined with imatinib decreases tumor cell proliferation. This synergistic effect was also shown using a Personal computer3 mouse tumor model: Combination of imatinib and radiotherapy only significantly delayed tumor growth, at least partially due to a decrease in RAD51 manifestation (24). The results of the present study shown that imatinib reduced RAD51 protein in ATL cells inside a dose- and time-dependent manner. Therefore, the combined treatment of imatinib and chemotherapeutic medicines HDM2 may be useful for the treatment of hematological tumors. Imatinib reduced the manifestation of RAD51, but the precise mechanism of how imatinib reduces RAD51 manifestation has not been fully elucidated; this requires further investigation in future experiments. For more far-reaching mechanisms, it will be necessary to determine the DNA damage response caused by RAD51 overexpression. In conclusion, the RAD51 protein is key to HR restoration pathways and was involved in the occurrence and drug resistance of leukemia. Improved manifestation of RAD51 recombination protein in various tumors is definitely a common trend (11). CPUY074020 Acute leukemia is definitely a malignancy with poor treatment results (3). Although RNAi technology focuses on gene activity by silencing and offers very high specificity, the medical software of siRNA is currently limited by its off-target effects and short life span. The limitations of this study include the lack of data from peripheral blood samples and a non-cancerous cell collection. In the present study, no normal peripheral blood samples or non-cancerous cell lines were used as bad controls; therefore, the experimental results can only show that RAD51 may serve an important part in blood tumor cell lines. In the present experiment, RAD51 knockdown decreased the restoration effectiveness of Jurkat cells and improved their chemosensitivity, ultimately leading to cell apoptosis. Based on these results, RAD51 appears to be promising like a novel target for the medical treatment of leukemia, and it may improve the survival of leukemia individuals. Acknowledgements Not relevant. Funding This study was supported by Ministry of Technology and Technology of China (grant no. 2016YFE0107200) and the National Natural Science Basis of China (grant no. 81770151). Availability of data and materials The datasets used and/or analyzed during the current study are available from your corresponding author on reasonable request. Authors’ contributions MY, XT and ZF designed the research and performed experiments. WY, ZL, WZ, JZ and AL collected the samples, and participated in the collection and analysis of data. XT published the manuscript. All authors read and authorized the final manuscript. Ethics authorization and consent to participate Not relevant. Patient consent for publication Not applicable. Competing interests The authors declare that they have no competing interests..