التفاصيل البيبلوغرافية
| العنوان: |
ZIC1 基因过表达激活 P53 信号通路抑制胸膜间皮瘤细胞增殖. (Chinese) |
| Alternate Title: |
Overexpression of ZIC1 Gene Inhibits Proliferation of Pleural Mesothelioma Cells by Activating P53 Signaling Pathway. (English) |
| المؤلفون: |
邓勇军, 陈 倩, 邹建彬, 宫 政, 刘焕鹏 |
| المصدر: |
Journal of Kunming Medical University / Kunming Yike Daxue Xuebao; 2024, Vol. 45 Issue 4, p35-40, 6p |
| Abstract (English): |
Objective To investigate the effect of cerebellar zinc finger structure 1 （ ZIC1） gene overexpression on the proliferation and apoptosis of pleural mesothelioma cells （SMC-1 cells） and the corresponding molecular mechanism. Methods SMC-1 cells were transfected with lentivirus particles carrying ZIC1 gene as the experimental group， infected with empty lentivirus particles as the control group， and conventional cultured untransfected SMC-1 cells as the blank control group. Western blot was used to detect the expression of ZIC1 protein in the three groups. CCK-8 cell proliferation assay was used to detect the proliferation ability of each group, and Hoechst-PI double staining was used to detect the apoptosis of each group. The protein expression levels of P53, P21, MDM2 and P53 phosphorylation site Ser392 in P53-mediated apoptosis signaling pathway were detected by Western blot. Results Compared with the empty vector group and the control group， the expression of ZIC1 protein in the ZIC1 overexpression group was significantly increased, with a statistically significant difference （F = 4.665， P = 0.036） . Compared with the control group, the proliferation ability of SMC-1 cells in the ZIC1 overexpression group was significantly reduced, while the apoptosis of tumor cells was significantly increased, with a statistically significant difference （ P < 0.05） . The main genes P53，P21，MDM2, and P53 Ser392 protein expression in the P53 signaling pathway in the ZIC1 gene overexpression group were significantly increased. Conclusion Overexpression of ZIC1 gene can inhibit the proliferation of pleural mesothelioma SMC-1 cells and promote their apoptosis. The possible mechanism is to activate the P53 gene mediated apoptosis signaling pathway by upregulating the expression of P53 gene phosphorylation sites. [ABSTRACT FROM AUTHOR] |
| Abstract (Chinese): |
目的 探讨小脑锌指结构 1（ZIC1） 基因过表达对胸膜间皮瘤 SMC-1 细胞增殖、凋亡的影响以及相 应的机制。方法 用携带 ZIC1 基因的慢病毒颗粒转染 SMC-1 细胞作为过表达组，用空载慢病毒颗粒感染 SMC)1 细胞作为空载体组，将常规培养未进行转染的 SMC-1 细胞作为空白对照组，采用 Western blot 在蛋白水平检 测 3 组细胞中 ZIC1 蛋白的表达情况；采用 CCK-8 细胞增殖试验检测各组细胞增殖能力，Hoechst-PI 双染法检 测各组细胞凋亡情况；采用 Western blot 检测 P53 介导的细胞凋亡信号通路的主要基因 P53、P21、MDM2 及 P53 磷酸化位点 Ser392 蛋白表达水平。结果 与空载组和对照组相比，ZIC1 过表达组中 ZIC1 蛋白的表达明显 增高，差异有统计学意义（F = 4.665，P = 0.036）；ZIC1 过表达组中肿瘤细胞的增殖活性明显减弱，而肿瘤细胞 的凋亡明显增加，差异有统计学意义（P < 0.05）；ZIC1 基因过表达组中 P53 信号通路中的主要基因 P53、P21、 MDM2 及 P53-Ser392 蛋白表达均明显增加（P < 0.05）。结论 ZIC1 基因过表达可以抑制胸膜间皮瘤 SMC-1 细胞 增殖，促进其凋亡，其可能的机制为通过上调 P53 基因磷酸化位点的表达激活 P53 基因介导的细胞凋亡信号通 路来实现。 [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |
