The Effect and Mechanism of Trachostatin A on Proliferation and Apoptosis of Chronic Myeloid Leukemia Cells
MOU Ke, PENG Yuhang, LI Qian, JIANG Guoyun, FENG Wenli*
In this paper, the effects of TSA (trichostatin A) and the possible mechanisms on proliferation and apoptosis of CML (chronic myeloid leukemia) cells K562 and K562/G01 were investigated. Different concentrations of TSA were used to treat K562 and K562/G01 cells. CCK8 and clone formation assay were used to detect the effect of TSA on cell proliferation. FCM (flow cytometry analysis), Western blot and DAPI staining were used to detect apoptosis; Western blot was used to detect the autophagy levels of cells and the levels of BCR-ABL/STAT5/c-Myc signal axis proteins after treated with TSA. The results showed that TSA could effectively inhibit the proliferation of K562 and K562/G01 cells, and significantly promote the apoptosis of K562 and K562/G01 cells. The combination of TSA and IM (imatinib) could more effectively kill CML cells. TSA inhibited the BCR-ABL/STAT5/c-Myc signal axis and reduced the c-Myc protein level. TSA enhanced the autophagy of CML cells. The autophagy inhibitor CQ (chloroquine) partially rescued the apoptosis caused by TSA. Those results indicated that TSA inhibited the proliferation of CML cells by suppressing the STAT5 signaling pathway and reducing the level ofc-Myc protein. Moreover, TSA enhanced CML cell autophagy and promoted cells apoptosis.
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