Department of Pediatrics, Guigang City People's Hospital, the Eight Affiliated Hospital of Guangxi Medical University, Guigang, P.R. China.
Department of Pediatrics, the First Affiliated Hospital of Guangxi Medical University, Nanning, P.R. China.
Ren Fail. 2021 Dec;43(1):1470-1478. doi: 10.1080/0886022X.2021.1994994.
The aim of present report was to elucidate the effect of cell division cycle associated 4 (CDCA4) on the proliferation and apoptosis of Wilm's tumor cells, and to further evaluate its underlying mechanism.
The expression profiles of CDCA4 and clinical information of Wilm's tumor patients were obtained from public Therapeutically Applicable Research to Generate Effective Treatments (TARGET) database portal. Real-time qPCR and western blot analyses were utilized to determine the expression levels of CDCA4. Gain- and loss-of-function of CDCA4 assays were conducted with transfection technology to investigate the biological role of CDCA4 in Wilm's tumor cells. Cell counting kit 8 and flow cytometer assays were employed to examine the effect of CDCA4 on the cells proliferation and apoptosis. Protein expression levels of indicated markers in each group of Wilm's tumor cells were measured by western blot.
The transcriptional expression of CDCA4 was drastically upregulated in Wilm's tumor tissues according to the public TARGET database and in Wilm's tumor cells. The cells viability was remarkably reduced whereas the cells apoptosis was increased in CDCA4-knockdown group compared with negative control group. However, CDCA4-overexpression group promoted the cells proliferation and suppressed the cells apoptosis. Furthermore, the protein expression levels of p-AKT, p-mTOR, and Cyclin D1 were significantly reduced after depletion of CDCA4, whereas overexpression of CDCA4 dramatically elevated these markers' expression levels.
CDCA4 is highly expressed in Wilm's tumor and promoted the proliferation whereas inhibited the apoptosis of Wilm's tumor cells through activating the AKT/mTOR signaling pathway.
本报告旨在阐明细胞分裂周期相关蛋白 4（CDCA4）对肾母细胞瘤细胞增殖和凋亡的影响，并进一步探讨其潜在机制。
从公共的治疗应用研究以产生有效的治疗方法（TARGET）数据库门户获取 CDCA4 的表达谱和肾母细胞瘤患者的临床信息。利用实时 qPCR 和 Western blot 分析来确定 CDCA4 的表达水平。通过转染技术进行 CDCA4 的增益和缺失功能实验，以研究 CDCA4 在肾母细胞瘤细胞中的生物学作用。细胞计数试剂盒 8 和流式细胞仪实验用于检测 CDCA4 对细胞增殖和凋亡的影响。通过 Western blot 测量每组肾母细胞瘤细胞中标记物的蛋白表达水平。
根据公共的 TARGET 数据库和肾母细胞瘤细胞中的数据，CDCA4 的转录表达在肾母细胞瘤组织中明显上调。与阴性对照组相比，CDCA4 敲低组的细胞活力明显降低，而细胞凋亡增加。然而，CDCA4 过表达组促进了细胞增殖并抑制了细胞凋亡。此外，CDCA4 耗尽后，p-AKT、p-mTOR 和 Cyclin D1 的蛋白表达水平显著降低，而过表达 CDCA4 则显著升高了这些标志物的表达水平。
CDCA4 在肾母细胞瘤中高表达，通过激活 AKT/mTOR 信号通路促进肾母细胞瘤细胞的增殖，抑制其凋亡。
