有丝分裂
细胞周期
生物
细胞生长
基因敲除
细胞凋亡
细胞生物学
流式细胞术
信号转导
细胞
癌细胞
癌症研究
分子生物学
癌症
遗传学
作者
Jinqiu Tao,Guangli Sun,Qing Li,Xiaofei Zhi,Hanjie Yu,Zhongyuan He,Huihui Chen,Aiping Zhou,Jiahui Ye,Guifang Xu,Wenxian Guan,Weijie Zhang
摘要
Abstract Kinesin family member 15 (KIF15) is a member of the kinesin superfamily of proteins, which promotes cell mitosis, participates in the transport of intracellular materials, and helps structural assembly and cell signaling pathways transduction. However, its biological role and molecular mechanisms of action in the development of gastric cancer (GC) remain unclear. In the present study, an integrated analysis of The Cancer Genome Atlas (TCGA), Gene Expression Omnibus database, and Kaplan–Meier plotter database was performed to predict the expression and prognostic value of KIF15 in GC patients. Detection of KIF15 expression in GC cells and tissues was performed by a quantitative polymerase chain reaction. In vitro cell proliferation, viability, colony formation ability and flow cytometry assays, and in vivo tumorigenicity assay, were performed to evaluate the effects of KIF15 knockdown on GC cell phenotype. It was demonstrated that the expression of KIF15 messenger RNA in GC tissues was significantly higher compared with that in adjacent tissues, and was closely associated with larger tumor size and poor patient prognosis. In addition, functional studies demonstrated that, due to the increase in reactive oxygen species (ROS) generation, the interference with the expression of KIF15 not only decreased cell proliferation but also increased cell apoptosis and induced cell cycle arrest. ROS‐mediated activation of c‐Jun N‐terminal kinase/c‐Jun signaling reduced cell proliferation by regulating the GC cell cycle and increasing apoptosis. Taken together, the results of the present study indicate that KIF15 is an oncoprotein contributing to GC progression, and is expected to help identify novel biomarkers and treatment targets in GC.
科研通智能强力驱动
Strongly Powered by AbleSci AI