Abstract：
UNASSIGNED: Arsenic has been reported to induce apoptosis in malignant tumor cells. Therefore, it has been investigated as a chemotherapy. From a mechanistic standpoint, the mitochondrial apoptosis pathway, mediated by GSK-3β, plays an important role in tumor cell apoptosis. Nonetheless, the regulation of GSK-3β by arsenic remains controversial. The study aimed to clarify the mechanism of GSK-3β in arsenic-induced apoptosis of tumor cells.
UNASSIGNED: We included 19 articles, which conducts the role of GSK-3β in the process of arsenic-induced tumor cell apoptosis by the meta-analysis.
UNASSIGNED: Compared with that of control group, the expression of GSK-3β (SMD= -0.92, 95% CI (-1.78, -0.06)), p-Akt (SMD= -5.46,95% CI (-8.67, -2.24)) were increased in the arsenic intervention group. Meanwhile, the combined treatment of arsenic and Akt agonists can inhibit p-GSK-3β. Using the dose and time subgroup analysis, it was shown that the low-dose (<5 μmol/L) and sub-chronic (>24 h) arsenic exposure could inhibit the expression of p-Akt (P < 0.05). In the subgroup analysis of GSK-3β sites, arsenic could inhibit p-Akt and GSK-3β (Ser9) (SMD = -0.95, 95% CI (-1.56, -0.33)). There was a positive dose-response relationship between arsenic and p-GSK-3β when the dose of arsenic was less than 8 μmol/L. The expression of Mcl-1 and pro-caspase-3 were decreased, while the loss of mitochondrial membrane potential and cleaved-caspase-3 increased significantly when arsenic stimulated GSK-3β (Ser9) (P < 0.05).
UNASSIGNED: The study revealed that arsenic could induce tumor cell apoptosis, by inhibiting p-Akt/GSK-3β, and triggering the Mcl-1-dependent mitochondrial apoptosis pathway.
UNASSIGNED: We included 19 articles, which conducts the role of GSK-3β in the process of arsenic-induced tumor cell apoptosis by the meta-analysis.
UNASSIGNED: Compared with that of control group, the expression of GSK-3β (SMD= -0.92, 95% CI (-1.78, -0.06)), p-Akt (SMD= -5.46,95% CI (-8.67, -2.24)) were increased in the arsenic intervention group. Meanwhile, the combined treatment of arsenic and Akt agonists can inhibit p-GSK-3β. Using the dose and time subgroup analysis, it was shown that the low-dose (<5 μmol/L) and sub-chronic (>24 h) arsenic exposure could inhibit the expression of p-Akt (P < 0.05). In the subgroup analysis of GSK-3β sites, arsenic could inhibit p-Akt and GSK-3β (Ser9) (SMD = -0.95, 95% CI (-1.56, -0.33)). There was a positive dose-response relationship between arsenic and p-GSK-3β when the dose of arsenic was less than 8 μmol/L. The expression of Mcl-1 and pro-caspase-3 were decreased, while the loss of mitochondrial membrane potential and cleaved-caspase-3 increased significantly when arsenic stimulated GSK-3β (Ser9) (P < 0.05).
UNASSIGNED: The study revealed that arsenic could induce tumor cell apoptosis, by inhibiting p-Akt/GSK-3β, and triggering the Mcl-1-dependent mitochondrial apoptosis pathway.
摘要：
未经证实：据报道，砷可诱导恶性肿瘤细胞凋亡。因此,它已经作为化疗进行了研究。从机械的角度来看，线粒体凋亡途径，由GSK-3β介导，在肿瘤细胞凋亡中起着重要作用。尽管如此，砷对GSK-3β的调控仍存在争议。本研究旨在阐明GSK-3β在砷诱导肿瘤细胞凋亡中的作用机制。
未经批准：我们收录了19篇文章，通过Meta分析研究GSK-3β在砷诱导肿瘤细胞凋亡过程中的作用。
UNASSIGNED：与对照组相比，GSK-3β的表达（SMD=-0.92，95%CI（-1.78，-0.06）），砷干预组p-Akt(SMD=-5.46,95%CI(-8.67,-2.24))升高。同时,砷和Akt激动剂联合治疗可抑制p-GSK-3β。使用剂量和时间亚组分析，结果表明，低剂量（<5μmol/L）和亚慢性（>24h）砷暴露可以抑制p-Akt的表达（P<0.05）。在GSK-3β位点的亚组分析中，砷可以抑制p-Akt和GSK-3β（Ser9）（SMD=-0.95，95％CI（-1.56，-0.33））。当砷的剂量小于8μmol/L时，砷与p-GSK-3β之间存在正的剂量-反应关系。Mcl-1和pro-caspase-3的表达降低,而当砷刺激GSK-3β（Ser9）时，线粒体膜电位和caspase-3的损失显着增加（P<0.05）。
未经证实：研究表明砷可诱导肿瘤细胞凋亡，通过抑制p-Akt/GSK-3β，并触发Mcl-1依赖性线粒体凋亡途径。
未经批准：我们收录了19篇文章，通过Meta分析研究GSK-3β在砷诱导肿瘤细胞凋亡过程中的作用。
UNASSIGNED：与对照组相比，GSK-3β的表达（SMD=-0.92，95%CI（-1.78，-0.06）），砷干预组p-Akt(SMD=-5.46,95%CI(-8.67,-2.24))升高。同时,砷和Akt激动剂联合治疗可抑制p-GSK-3β。使用剂量和时间亚组分析，结果表明，低剂量（<5μmol/L）和亚慢性（>24h）砷暴露可以抑制p-Akt的表达（P<0.05）。在GSK-3β位点的亚组分析中，砷可以抑制p-Akt和GSK-3β（Ser9）（SMD=-0.95，95％CI（-1.56，-0.33））。当砷的剂量小于8μmol/L时，砷与p-GSK-3β之间存在正的剂量-反应关系。Mcl-1和pro-caspase-3的表达降低,而当砷刺激GSK-3β（Ser9）时，线粒体膜电位和caspase-3的损失显着增加（P<0.05）。
未经证实：研究表明砷可诱导肿瘤细胞凋亡，通过抑制p-Akt/GSK-3β，并触发Mcl-1依赖性线粒体凋亡途径。
