Implications of cell division cycle associated 4 on the Wilm's tumor cells viability via AKT/mTOR signaling pathway

细胞分裂周期相关 4 通过 AKT/mTOR 信号通路对 Wilm 肿瘤细胞活力的影响

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作者:Suqing Li, Cong Qin, Yike Chen, Dan Wei, Zhijun Tan, Jiadong Meng

Conclusions

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.

Methods

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.

Objective

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.

Results

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. Conclusions: 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.

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