| 韩萍萍,王怀宇,蔡 云,孙 烨,夏欣欣,刘 昳,胡 珊,周冬枝.复元胜白方通过调控JAK2/STAT3通路抑制急性髓系白血病细胞恶性生物学行为[J].,2024,(15):2817-2823 |
| 复元胜白方通过调控JAK2/STAT3通路抑制急性髓系白血病细胞恶性生物学行为 |
| FYSBF Inhibited the Malignant Biological Behavior of Acute Myeloid Leukemia Cells by Regulating JAK2/STAT3 Pathway |
| 投稿时间：2024-02-28 修订日期：2024-03-23 |
| DOI：10.13241/j.cnki.pmb.2024.15.003 |
| 中文关键词: 复元胜白方 JAK2/STAT3通路 急性髓系白血病 增殖 侵袭 |
| 英文关键词: Fu Yuan Sheng Bai Fang (FYSBF) JAK2/STAT3 Acute myeloid leukemia (AML) Proliferation Invasion |
| 基金项目:陕西省中医药管理局委托办事经费项目（ZYJXG-L23020）；陕西省重点研发计划项目（2024SF-YBXM-521） |
|
| 摘要点击次数: 101 |
| 全文下载次数: 62 |
| 中文摘要: |
| 摘要 目的：探究复元胜白方（FYSBF）对急性髓系白血病（AML）的治疗作用与JAK/STAT信号通路的关系及机制。方法：将AML细胞系HL-60细胞分为对照组、FYSBF组、IL-6组（IL-6为JAK/STAT信号通路激活剂）和FYSBF+IL-6组。对照组HL-60细胞采用正常RPMI 1640培养基培养，FYSBF组HL-60细胞的培养基中添加终浓度为200 μg/mL的FYSBF，IL-6组HL-60细胞的培养基中添加终浓度为100 ng/mL的IL-6，FYSBF+IL-6组HL-60细胞的培养基中添加终浓度为200 μg/mL的FYSBF和100 ng/mL的IL-6。采用CCK-8法和克隆形成实验检测细胞增殖水平，流式细胞术检测细胞周期分布和细胞凋亡水平，Transwell实验检测细胞侵袭和迁移水平，Western blot实验分析蛋白表达水平。结果：与对照组比较，FYSBF组HL-60细胞相对活力、克隆数量、迁移和侵袭细胞数量以及S期细胞比例均降低（P<0.05），CDK2、cyclin E、N-cadherin和Vimentin的蛋白表达量均降低（P<0.05），JAK2和STAT3蛋白的磷酸化水平均降低（P<0.05），G0/G1期细胞比例和细胞凋亡率均升高（P<0.05），p21和E-cadherin的蛋白表达量均升高（P<0.05）。与对照组比较，IL-6组HL-60细胞相对活力、克隆数量、迁移和侵袭细胞数量以及S期细胞比例均升高（P<0.05），CDK2、cyclin E、N-cadherin和Vimentin的蛋白表达量均升高（P<0.05），JAK2和STAT3蛋白的磷酸化水平均升高（P<0.05），G0/G1期细胞比例和细胞凋亡率均降低（P<0.05），p21和E-cadherin的蛋白表达量均降低（P<0.05）。与IL-6组比较，FYSBF+IL-6组HL-60细胞相对活力、克隆数量、迁移和侵袭细胞数量以及S期细胞比例均降低（P<0.05），CDK2、cyclin E、N-cadherin和Vimentin的蛋白表达量均降低（P<0.05），JAK2和STAT3蛋白的磷酸化水平均降低（P<0.05），G0/G1期细胞比例和细胞凋亡率均升高（P<0.05），p21和E-cadherin的蛋白表达量均升高（P<0.05）。结论：复元胜白方通过抑制JAK2/STAT3通路激活，进而抑制急性髓系白血病细胞增殖、迁移、侵袭和上皮-间质转化，促进细胞凋亡和细胞周期阻滞。 |
| 英文摘要: |
| ABSTRACT Objective: To explore the relationship between the therapeutic effect of Fu Yuan Sheng Bai Fang (FYSBF) on acute myeloid leukemia (AML) and the JAK/STAT signaling pathway and its mechanism. Methods: AML HL-60 cells were divided into control group, FYSBF group, IL-6 group (IL-6 is the activator of JAK/STAT signaling pathway) and FYSBF+IL-6 group. HL-60 cells in control group were cultured in normal RPMI 1640 medium, HL-60 cells in FYSBF group were cultured in medium which was added with a final concentration of 200 μg/mL FYSBF, and HL-60 cells in IL-6 group were cultured in medium which was added with a final concentration of 100 ng/mL IL-6. HL-60 cells in FYSBF+IL-6 group were cultured in medium which were added with final concentration of 200 μg/mL FYSBF and 100 ng/mL IL-6. The cell proliferation was detected by CCK-8 assay and clonal formation assay, cell cycle distribution and apoptosis were detected by flow cytometry, cell invasion and migration were detected by Transwell assay, and protein expression levels were analyzed by Western blot assay. Results: Compared with the control group, the relative vitality, number of clones, number of migration and invasion cells and proportion of S-phase cells in FYSBF group were decreased (P<0.05), and the protein expressions of CDK2, cyclin E, N-cadherin and Vimentin were decreased (P<0.05), the phosphorylation levels of JAK2 and STAT3 proteins were decreased (P<0.05), the cells proportion of G0/G1 phase and apoptosis rate were increased (P<0.05), and the protein expression of p21 and E-cadherin were increased (P<0.05). Compared with the control group, the relative vitality, number of clones, number of migration and invasion cells and proportion of S-phase cells in IL-6 group were increased (P<0.05), and the protein expressions of CDK2, cyclin E, N-cadherin and Vimentin were increased (P<0.05), the phosphorylation levels of JAK2 and STAT3 proteins were increased (P<0.05), the cells proportion of G0/G1 phase and apoptosis rate were decreased (P<0.05), and the protein expression of p21 and E-cadherin were decreased (P<0.05). Compared with the IL-6 group, the relative vitality, number of clones, number of migration and invasion cells and proportion of S-phase cells in FYSBF+IL-6 group were decreased (P<0.05), and the protein expressions of CDK2, cyclin E, N-cadherin and Vimentin were decreased (P<0.05), the phosphorylation levels of JAK2 and STAT3 proteins were decreased (P<0.05), the cells proportion of G0/G1 phase and apoptosis rate were increased (P<0.05), and the protein expression of p21 and E-cadherin were increased (P<0.05). Conclusion: FYSBF can inhibit the proliferation, migration, invasion and epithelial-mesenchymal transformation of acute myeloid leukemia cells, and promote cell apoptosis and cell cycle arrest, which may be related to inhibiting the activation of JAK2/STAT3 pathway. |
|
查看全文
查看/发表评论 下载PDF阅读器 |
| 关闭 |
|
|
|
