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首页> 外文期刊>Cellular Physiology and Biochemistry >The Role of the Globular Heads of C1q Receptor (gC1qR) Gene in Regulating Apoptosis of Human Cervical Squamous Cell Carcinoma
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The Role of the Globular Heads of C1q Receptor (gC1qR) Gene in Regulating Apoptosis of Human Cervical Squamous Cell Carcinoma

机译:C1q受体(gC1qR)基因的球状头在调节人类宫颈鳞状细胞癌细胞凋亡中的作用

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摘要

Background: The globular heads of the human C1q receptor (gC1qR) are multi-compartmental and multi-functional cellular proteins. The list of biological responses mediated by the gC1qR includes growth perturbation and morphological abnormalities, along with the initiation of apoptosis. However, the effects of the gC1qR on the apoptosis of cervical squamous carcinoma cells (C33a and SiHa) have not been demonstrated. Methods: Here, human cervical tissues were examined for the expression of the gC1qR using real-time PCR and Western blot analysis. Apoptotic death of C33a and SiHa cells was assessed by flow cytometric analysis to detect the subG1 population. Viability, migration and proliferation of C33a and SiHa cells were detected via the water-soluble tetrazolium salt (WST-1) assay, the Transwell assay and the 3H-thymidine incorporation into DNA assay (~3H-TdR), respectively. Results: These data showed that expression of the gC1qR protein was significantly decreased in human cervical squamous cell carcinoma tissues relative to normal cervix tissues. C33a and SiHa cells transfected with a GFP-gC1qR vector resulted in the up-regulation of cellular apoptosis and an apparent increase in the expression of the p38 mitogen-activated protein kinase (p38 MAPK). Further, the changes in C33a and SiHa cells viability, migration and proliferation observed upon overexpression of gC1qR could be abrogated using the p38 MAPK inhibitor SB202190. Conclusion: These data indicate that gC1qR inhibits viability, migration and proliferation of cervical squamous cells carcinoma via the p38 MAPK signalling pathway.
机译:背景:人类C1q受体(gC1qR)的球形头部是多隔室和多功能的细胞蛋白。由gC1qR介导的生物学反应包括生长扰动和形态异常,以及细胞凋亡的启动。但是,尚未证明gC1qR对宫颈鳞状细胞癌细胞(C33a和SiHa)凋亡的影响。方法:在这里,使用实时荧光定量PCR和Western印迹分析技术检测人宫颈组织中gC1qR的表达。通过流式细胞仪分析评估C33a和SiHa细胞的凋亡死亡,以检测subG1群体。分别通过水溶性四唑盐(WST-1)测定,Transwell测定和将3H-胸苷掺入DNA测定(〜3H-TdR)检测C33a和SiHa细胞的活力,迁移和增殖。结果:这些数据表明,在人宫颈鳞状细胞癌组织中,相对于正常宫颈组织,gC1qR蛋白的表达显着降低。用GFP-gC1qR载体转染的C33a和SiHa细胞导致细胞凋亡的上调,并且p38促分裂原活化蛋白激酶(p38 MAPK)的表达明显增加。此外,使用p38 MAPK抑制剂SB202190可以消除在过度表达gC1qR时观察到的C33a和SiHa细胞活力,迁移和增殖的变化。结论:这些数据表明gC1qR通过p38 MAPK信号通路抑制宫颈鳞状细胞癌的活力,迁移和增殖。

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