Kang Hongyang, Tong Changqing, Li Chaonan, Luo Jianmin
Department of Hematology, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Department of Hematology, The First Affiliated Hospital of Hebei North University, Zhangjiakou, China.
Cytotechnology. 2020 Jun;72(3):427-432. doi: 10.1007/s10616-020-00389-5. Epub 2020 Mar 11.
Acute myelod leukemia (AML), as a uncontrolled proliferation of cells, was arrested differentiation of progenitor cells. The present study aimed to explore Tanshinone IIA (TIIA) effects on OCI-AML3 and the involvement of the MAPK signaling pathway and miR-497 in TIIA-mediated effects. Cell growth percentage was detected using a cell counting kit. Expression of miR-497 was detected by qPCR. Phosphorylated ERK1/2, JNK and p38 were assessed using western blot. The growth percentage of OCI-AML3 decreased and the effected time increased with increasing TIIA concentration. The miR-497 was upregulated and the p-ERK1/2 was decreased when the TIIA added. TIIA cannot influence the p-ERK1/2. Hence, the proliferation of OCI-AML3 cells was raising. However, when the p-ERK1/2 was inhibited, there no influence on the miR-497 expression after TIIA added. TIIA upregulates miR-497, and decrease the p-ERK1/2 expression, when TIIA simulated OCI-AML3 cell in vitro. And in miR-497 might be involved in the regulation of proliferation in this process.
急性髓系白血病（AML）是一种细胞不受控制的增殖，其祖细胞分化受阻。本研究旨在探讨丹参酮IIA（TIIA）对OCI-AML3细胞的作用以及丝裂原活化蛋白激酶（MAPK）信号通路和miR-497在TIIA介导作用中的参与情况。使用细胞计数试剂盒检测细胞生长百分比。通过定量聚合酶链反应（qPCR）检测miR-497的表达。使用蛋白质免疫印迹法评估磷酸化的细胞外信号调节激酶1/2（ERK1/2）、应激活化蛋白激酶（JNK）和p38。随着TIIA浓度的增加，OCI-AML3细胞的生长百分比降低，作用时间延长。添加TIIA后，miR-497上调，p-ERK1/2降低。TIIA不影响p-JNK和p-p38。因此，OCI-AML3细胞的增殖受到抑制。然而，当抑制p-ERK1/2时，添加TIIA后对miR-497的表达没有影响。在体外模拟OCI-AML3细胞时，TIIA上调miR-497，并降低p-ERK1/2的表达。并且miR-497可能参与了这一过程中细胞增殖的调控。
