Downregulation of KIF20A induces cell cycle arrest and apoptosis by suppressing PI3K/AKT in human glioblastoma

被引:0
|
作者
Wang, Min [1 ,2 ]
Liu, Kun [3 ]
Zhou, Xin-Ling [4 ]
Mei, Shu-Yu [1 ]
Zhang, Cui-Juan [1 ]
Zhang, Ting-Guo [1 ]
机构
[1] Shandong Univ, Sch Med, Dept Pathol, Wenhuaxi Rd 44, Jinan 250012, Shandong, Peoples R China
[2] Second Peoples Hosp Liaocheng, Dept Pathol, Linqing 252601, Shandong, Peoples R China
[3] Second Peoples Hosp Liaocheng, Dept Neurosurg, Linqing 252601, Shandong, Peoples R China
[4] Second Peoples Hosp Liaocheng, Dept Obstet & Gynecol, Linqing 252601, Shandong, Peoples R China
关键词
KIF20A; glioblastoma; cell proliferation; cell migration; cell cycle; PI3K/Akt pathway; SUPERFAMILY PROTEINS; SIGNALING PATHWAY; KINESIN; CANCER; PROLIFERATION; TRANSPORT; PROGNOSIS; GENISTEIN;
D O I
暂无
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Background/Aim: Aberrant function of the kinesin family member 20A (KIF20A) has been reported to be vital in tumor genesis and development. However, the role of KIF20A in cell proliferation and invasion, as well as the mechanism underlying cell cycle arrest, remains unclear. Materials and Methods: Here, we first measured the expression of KIF20A in malignant astrocytoma and glioblastoma cell lines by immunohistochemistry and western blotting. Next, we knocked down KIF20A expression using siRNA to study its effect on cell proliferation and cycle. Results: We found that KIF20A knock down significantly suppressed cell proliferation, migration and invasion of glioblastoma cells. Importantly, KIF20A knock down induced cell cycle arrest in G0/G1 phase and promoted apoptosis by inactivating the PI3K/Akt pathway via c-Myc and activating the intrinsic apoptosis pathway. Conclusion: Taken together, our results suggest that KIF20A down-regulation can inhibit glioma tumorigenesis, which may provide a therapeutic target for treating glioma.
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页码:16133 / +
页数:13
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