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The Effect of TRAF6 Knockdown on Proliferation and Apoptosis of K562 Leukemia Cells and Its Molecular Mechanism
Zhang Shuaishuai, Xian Jingrong, Zou Qin, Quan Jing, Jin Hongjun, Gao Peng, Ye Sheng, Zhang Ling*
College of Laboratory Medicine, Key Laboratory of Laboratory Medical Diagnostics Designated by the Ministry of Education, Chongqing Medical University, Chongqing 400016, China
Abstract: This work was aim to investigate the effect of TRAF6 knockdown on proliferation and apoptosis of human K562 leukemic cell line and its molecular mechanism. In this study， the shRNA targeting TRAF6 lentiviral vector was transfected into K562 leukemia cells. The efficiency of transfection was observed under fluorescence microscope. The change of TRAF6 protein level was confirmed by Western blot. The ability of cell proliferation were analyzed by CCK-8 method and the apoptosis rate were detected by flow cytometry. The expressions of apoptosis related proteins Bax， Bcl-2 and phosphorylated-AKT were detected by Western blot. The results demonstrated that TRAF6-shRNA was successfully transfected into K562 cells and knockdown of TRAF6 at the protein levels was confirmed. Compared with the blank control group and the TRAF6-NC group， the cell growth in the TRAF6-shRNA group was significantly inhibited (P<0.05). In addition， knockdown of TRAF6 promoted apoptosis by increasing the protein level of Bax and decreasing the Bcl-2. Furthermore， TRAF6 downregulation resulted in the decreases in levels of AKT phosphorylation at both residues Thr308 and Ser473， but no remarkable change in total AKT levels was observed. Taken together， our results revealed that TRAF6 knockdown might inhibit cell growth and induce apoptosis through downregulation of AKT activation， which indicates that TRAF6 may be a novel target for leukemia treatment.
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