Combined Effect of Bortezomib and Homoharringtonine on K562 Cells and their Mechanisms / 中国实验血液学杂志

<p><b>OBJECTIVE</b>To explore the effects of BTZ plus HHT on proliferation and apoptosis of K562 cells, and to clarify the relationship between the mechanism inderlying the effect of BTZ plus HHT on K562 cells and BCL-2, BAX, MCL-1 proteins.</p><p><b>METHODS</b>The K562 cells were divided into 4 groups by different treatment: BTZ(20 nmol/L), HHT(40 ng/ml), BTZ(20 nmol/L)+HHT(40 ng/ml) and control. The proliferation inhibition rates of K562 cells in each group were detected by using MTT, and the early apoptosis rates of K562 cells in each group were assayed by using flow cytometry with Annexin V-FITC/PI staining. The proteins level of BCL-2, BAX and MCL-1 in each group were examined by using Western blot.</p><p><b>RESULTS</b>The inhibition rate of K562 cell proliferation in combined group was higher than that in BTZ, HHT alone group(P<0.01). The early apoptosis rate of K562 cells in combined group was increased significantly in comparison with BTZ and HHT alone group(P<0.05). The BCL-2 protein level of K562 cells in combined group was significantly lower than that in BTZ and HHT alone group(P<0.05). BAX protein level of K562 cells in combined group was higher than that in BTZ and HHT alone group(P<0.05). The Orders of the MCL-1 protein level of K562 cells in 4 groups were BTZ>Control>BTZ plus HHT>HHT(P<0.05 ).</p><p><b>CONCLUSION</b>The combination of BTZ and HHT exerts the synergistic effect of anti-proliferative activity and induces apoptosis against K562 cells in vitro. The combination can induce apoptosis of K562 cells via suppression of BCL-2 protein and up-regulation of BAX protein. HHT can increase the sensitivity of K562 cells to BTZ by down-regulating the expression of MCL-1 protein.</p>

Expression of miR-155 in Acute Myeloid Leukemia and Its Clinical Significance / 中国实验血液学杂志

<p><b>OBJECTIVE</b>To investigate the expression of microRNA-155(miR-155) in bone marrow mononuclear cells (BMMNC) of the patients with acute myeloid leukemia(AML) and its clinical significance.</p><p><b>METHODS</b>Real-time quantitative PCR (qPCR) was used to detect the expression level of miR-155 in bone marrow mononuclear cells from 80 cases of AML and 11 cases of negative control patients.</p><p><b>RESULTS</b>Compared with the negative control group ,the expressions of miR-155 in initial diagnosis group and remission group both increased (P<0.01), that in the initial treatment group was significantly higher than the remission group (P<0.05). The expression level of miR-155 did not significantly correlate with the clinical features of patients. Between different cytogenetic groups in AML patients, miR-155 expression levels in the moderate prognostic group and poor prognositic group were significantly higher as compared with the favorable prognosis group P<0.05, P<0.05）, but there was no significant difference between poor and moderate progrestic groups(P>0.05). The results of tracking the situation after induction therapy of newly diagnozed AML patients showed that the remission rate of initial induction in miRNA155 high expression group and low expression group were 59.09% and 87.5% (X(2) =4.8, P<0.05), and the expression level of miR-155 in initial diagnosis of patients without complete remission after chemotherapy was significantly higher than that in patients with complete remission after chemotherapy (P= 0.042).</p><p><b>CONCLUSION</b>The expression of miR-155 in AML patients is high and reduced the rate of complete remission. The high expression of miR-155 is an poor prognostic factor for patients with AML.</p>