KIFC1 overexpression promotes prostate cancer cell survival and proliferation in vitro by clustering of amplified centrosomes via interaction with Centrin 2
作者机构：The Sperm LaboratoryCollege of Life SciencesZhejiang UniversityHangzhou310058China The First Affiliated HospitalCollege of MedicineZhejiang UniversityHangzhou310003China Department of Biotechnology and Genetic EngineeringFaculty of Biological SciencesIslamic UniversityKushtia7003Bangladesh
出 版 物：《BIOCELL》 (生物细胞（英文）)
年 卷 期：2021年第45卷第5期
页 面：1369-1391页
核心收录：
学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
基 金：Natural Science Foundation of Zhejiang Province China(No.LY20H040010)
主 题：KIFC1 Centrosome clustering Centrosome amplification Prostate cancer
摘 要：Mitotic kinesin KIFC1 plays critical roles in mitosis by regulating the spindle length,pole formation,and known for clustering extra centrosomes in cancer *** clustering is associated with the survival of cancer cells,but this phenomenon remains obscure in prostate cancer(PCa).The present study demonstrated that PCa cells showed centrosome amplification and clustering during interphase and mitosis,***1 is highly expressed in PCa cells and tumor tissues of prostatic adenocarcinoma(PAC)***-regulation of KIFC1 facilitated the PCa cell survival in vitro by ensuring bipolar mitosis through clustering the multiple centrosomes,suggesting centrosome clustering could be a leading cause of prostate ***,the silencing of KIFC1 resulted in normal centrosome number or multipolar mitosis by inhibiting the clustering of amplified centrosomes in PCa ***,knockdown of KIFC1 by RNAi in PCa cells reduced cancer cell survival,and ***1 interacted with centrosome structural protein Centrin 2 in clustering of amplified centrosomes in PCa cells to ensure the bipolar mitotic spindle *** of Centrin 2 in PCa cells inhibited the centrosome amplification and ***,up-regulated KIFC1 promotes PCa cell proliferation via progression of cell cycle possibly through aberrant activation of cyclin dependent kinase 1(Cdk1).Therefore,KIFC1 can be a prognostic marker and therapeutic target of PCa for inhibiting the cancer cell proliferation.
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