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首页> 外文期刊>Cellular Physiology and Biochemistry >The Critical Role of PTEN/PI3K/AKT Signaling Pathway in Shikonin-Induced Apoptosis and Proliferation Inhibition of Chronic Myeloid Leukemia
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The Critical Role of PTEN/PI3K/AKT Signaling Pathway in Shikonin-Induced Apoptosis and Proliferation Inhibition of Chronic Myeloid Leukemia

机译：PTEN / PI3K / AKT信号通路在紫草素诱导的慢性粒细胞白血病的细胞凋亡和增殖抑制中的关键作用

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Background/Aims Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm. Tyrosine kinase inhibitors (TKIs) are commonly used to treat CML; however, drug resistance of CML cells to TKIs has limited their clinical application. Shikonin, a traditional Chinese herb, has long been used to treat leukemia in China, but the roles and related molecular mechanisms of shikonin treatment in CML remain unclear. Here, we aimed to evaluate the effects of shikonin on the proliferation, apoptosis, and migration of K562 cells, a CML cell line. Methods Firstly, K562 cell proliferation and apoptosis were tested by CCK8 assay and flow cytometry with Annexin V-FITC/PI staining. Cell migration was measured by Transwell migration assay. In addition, western blot was performed to determine the proteins (PI3K, Bax, Bcl-2, cleaved caspase-3, PTEN, p-AKT, AKT, CXCR4, SDF-1, CD44) involved in the mechanism of action of shikonin. Finally, neutrophils from peripheral blood of CML patients were obtained, and cell proliferation and apoptosis were tested by CCK8 assay and flow cytometry. Results Shikonin reduced the proliferation of K562 cells in a time- and dose-dependent manner and promoted the apoptosis of K562 cells. Moreover, shikonin increased the PTEN level and inactivated the PI3K/AKT signaling pathway, subsequently upregulating BAX in K562 cells. In addition, shikonin could block K562 cell migration via the CXCR4/SDF-1 axis. Finally, shikonin significantly inhibited the proliferation and promoted the apoptosis of neutrophils from CML patients. Conclusion These results demonstrated that shikonin inhibits CML proliferation and migration and induces apoptosis by the PTEN/PI3K/AKT pathway, revealing the effects of shikonin therapy on CML.
机译：背景/目的慢性粒细胞白血病（CML）是一种骨髓增生性肿瘤。酪氨酸激酶抑制剂（TKIs）通常用于治疗CML。但是，CML细胞对TKI的耐药性限制了其临床应用。紫草素是中国的一种传统草药，长期以来一直用于治疗白血病，但紫草素在CML中的作用和相关的分子机制仍不清楚。在这里，我们旨在评估紫草素对CML细胞系K562细胞的增殖，凋亡和迁移的影响。方法首先通过CCK8法和膜联蛋白V-FITC / PI染色流式细胞术检测K562细胞的增殖和凋亡。通过Transwell迁移测定法测量细胞迁移。另外，进行蛋白质印迹法以确定参与紫草素作用机理的蛋白（PI3K，Bax，Bcl-2，裂解的胱天蛋白酶-3，PTEN，p-AKT，AKT，CXCR4，SDF-1，CD44）。最后，获得了CML患者外周血中性粒细胞，并通过CCK8测定和流式细胞术检测了细胞的增殖和凋亡。结果紫草素以时间和剂量依赖性的方式减少了K562细胞的增殖，并促进了K562细胞的凋亡。此外，紫草素增加了PTEN水平并灭活了PI3K / AKT信号通路，随后上调了K562细胞中的BAX。此外，紫草素可以通过CXCR4 / SDF-1轴阻止K562细胞迁移。最后，紫草素显着抑制了CML患者中性粒细胞的增殖并促进了其凋亡。结论这些结果表明，紫草素通过PTEN / PI3K / AKT途径抑制CML增殖和迁移并诱导细胞凋亡，揭示了紫草素治疗对CML的影响。

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