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Inhibitory Effect on Proliferation of K562 Cells by Transporting BCR-ABL into Nucleus with FKBP-RAP-FRB System
Gao Miao, Huang Zhenglan, Cao Weixi, Li Qianyin, Li Hui, Feng Wenli*
Department of Clinical Hematology, Key Laboratory of Medical Diagnostics, Ministry of Education, Chongqing Medical University, Chongqing 400016, China
Abstract: BCR-ABL fusion protein is demonstrated as the pathogenesis of chronic myeloid leukemia (CML). Failure of cytoplasmic BCR-ABL translocating into nucleus plays a key role. Therefore， transporting BCR-ABL into nucleus may be a potential therapeutic approach of CML. In this study， HA-2FKBP-ABD (HF2A) and FLAG-3NLS-FRB* (FN3R) recombinant adenovirus were constructed by recombinant DNA technology. HF2A， FN3R， and rapamycin analog constituted FKBP-RAP-FRB system， which was used to transport cytoplasmic BCR-ABL oncoprotein into nucleus. By this mean， the effect on the proliferation of K562 cells was detected. Our results showed that high titer of recombinant adenovirus were successfully constructed， and the target protein was successfully expressed in K562 cells confirmed by Western blot. FKBP-RAP-FRB system could inhibit growth and colony formation of K562 cells by transporting BCR-ABL into nucleus. These results revealed that FKBP-RAP-FRB system transporting BCR-ABL into nucleus could provide new insights for the treatment of CML.
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