title: Inhibition of KIF14 Suppresses Tumor Cell Growth and Promotes Apoptosis in Human Glioblastoma.
abstract: OBJECTIVE
  The mitotic kinesin superfamily protein KIF14 is essential for cytokinesis and chromosome segregation, and increased KIF14 expression is related to a variety of human cancers. However, the role of KIF14 in the development and malignant progression of astrocytomas and the underlying mechanisms remain unclear. The present study examined the relation between KIF14 and the pathogenesis of malignant astrocytoma.
  
  
  RESULTS
  The role of KIF14 in astrocytoma development and progression was investigated by analyzing KIF14 expression using SYBR Green quantitative real-time RT-PCR, western blotting and immunohistochemistry in human astrocytoma and normal brain tissues. KIF14 expression was higher in astrocytoma samples, and was positively correlated with pathological grade and proliferative activity indicated by Ki-67 staining. SiRNA knockdown of KIF14 inhibited tumor growth in vitro and in vivo, attenuated anchorage-independent growth, and induced G2/M phase arrest, cytokinesis failure and apoptosis in glioblastoma cell lines in association with decreased AKT phosphorylation and activity.
  
  
  CONCLUSIONS
  The upregulation of KIF14 in astrocytoma is associated with disease severity, and suppression of KIF14 inhibits cell proliferation and induces apoptosis through a mechanism involving the inactivation of AKT signaling, suggesting that KIF14 plays an important role in astrocytoma tumorigenesis and could be a promising molecular target for anticancer therapy.
authors.forename: Wei
authors.initials: W
authors.lastname: Huang
authors.forename: JunYu
authors.initials: J
authors.lastname: Wang
authors.forename: Danfeng
authors.initials: D
authors.lastname: Zhang
authors.forename: Wen
authors.initials: W
authors.lastname: Chen
authors.forename: Lijun
authors.initials: L
authors.lastname: Hou
authors.forename: Xiaojun
authors.initials: X
authors.lastname: Wu
authors.forename: Yicheng
authors.initials: Y
authors.lastname: Lu
mesh_terms: D000368:Aged; D017209:Apoptosis; D001921:Brain / Q000378:metabolism / Q000473:pathology; D001932:Brain Neoplasms / Q000378:metabolism / Q000473:pathology*; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D005260:Female; D059565:G2 Phase Cell Cycle Checkpoints; D005909:Glioblastoma / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D019394:Ki-67 Antigen / Q000378:metabolism; D016547:Kinesins / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D059566:M Phase Cell Cycle Checkpoints; D008297:Male; D008875:Middle Aged; D015513:Oncogene Proteins / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D034622:RNA Interference; D034741:RNA, Small Interfering / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D019394:Ki-67 Antigen; D015513:Oncogene Proteins; D034741:RNA, Small Interfering; D051057:Proto-Oncogene Proteins c-akt; C502598:KIF14 protein, human; D016547:Kinesins