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Effects of Lapatinib on Cell Proliferation and Apoptosis in NB4 Cells


Liu Lu1,2, Liu Beizhong1,2, Zhao Yi1, Chen Min1, Yao Shifei1, Li Lianwen1, Xiao Chunlan1, Shan Zhiling2, Xu Ting1, Gan Liugen1, Zhong Liang2*
1Central Laboratory of Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China; 2Key Laboratory of Laboratory Medical Diagnostics, Ministry of Education Faculty of Laboratory Medicine, Key Laboratory of Chongqing, Chongqing Medical University, Chongqing 400016, China
Abstract: This study was aimed to investigate the effect of lapatinib on cell proliferation and apoptosis in NB4 cells, and its related mechanisms. NB4 cells were treated with p38MAPK inhibitor and different concentrations of lapatinib for 24 h. The proliferation of NB4 cells was detected by CCK-8 (cell counting kit-8) assay. Apoptosis was determined by Annexin V/PI double binding assay and Hoechst 33258 fluorescent staining. Morphological changes were observed under optical microscope. The protein levels of Bcl-2 (B cell leukemia-2), Bax (Bcl-2 associated X protein), caspase-3, PARP (poly-ADP-ribose polymerase), PML-RARα (promyelocytic leukemia retinoic acid receptor alpha), p38MAPK (p38 mitongen-activated protein kinase) and p-p38MAPK (phosphorylated p38 mitongen-activated protein kinase) were detected by Western blot. The results showed that lapatinib significantly inhibited proliferation and induced apoptosis of NB4 cells. Chromatin condensation and fragmentation were observed in lapatinib treated group. Lapatinib decreased the levels of Bcl-2 and PML-RARα, increased the levels of Bax, cleaved caspase-3, cleaved PARP and p-p38MAPK. Meanwhile, SB203580 partially increase the viability of NB4 cells and reduced apoptosis induced by lapatinib; and decreased the levels of p-p38MAPK, Bax, cleaved caspase-3 and cleaved PARP. These results suggested that lapatinib inhibited proliferation and induced apoptosis in NB4 cells, and p38MAPK signal pathway may be involved in these processes.


CSTR: 32200.14.cjcb.2017.11.0003