title: Silencing Kif2a induces apoptosis in squamous cell carcinoma of the oral tongue through inhibition of the PI3K/Akt signaling pathway.
abstract: Previous studies have demonstrated that the overexpression of Kif2a is involved in the progression, invasion and metastasis of squamous cell carcinoma of the oral tongue (SCCOT). Few studies have reported the correlation between Kif2a and apoptosis of tumor cells and which signaling pathways Kif2a is involved in remains unclear. The phosphatidylinositol‑3‑kinase (PI3K)/protein kinase B (Akt) pathway is frequently activated in many types of human cancer. The aim of the present study was to investigate the effects of downregulation of Kif2 expression on the P13K/Akt pathway in Tca8113 cells to determine whether silencing of Kif2 inhibits the P13K/Akt pathway, resulting in cell apoptosis. siRNA vector was constructed, western blot analysis was used to determine RNA interference and flow cytometry was used to determine promotion of Tca8113 cell apoptosis. The results revealed that silencing Kif2a induces apoptosis and decreases the mRNA and protein level of PI3K, Akt and B‑cell lymphoma 2 (Bcl‑2) in Tca8113 cells. The PI3K-specific agonist insulin‑like growth factor 1 (IGF‑1) eliminated the upregulation of apoptosis of Tca8113‑Kif2a cells by phosphorylation of Akt. The results suggest that silencing Kif2a induces tumor cell apoptosis, at least partially, through the PI3K/Akt signaling pathway.
authors.affiliation: Department of Oral and Maxillofacial Surgery and Institution of Dental Medicine, Qilu Hospital, Shandong University, Jinan, Shandong 250012, P.R. China.
authors.forename: Ketao
authors.initials: K
authors.lastname: Wang
authors.forename: Changlong
authors.initials: C
authors.lastname: Lin
authors.forename: Chengqin
authors.initials: C
authors.lastname: Wang
authors.forename: Qianqian
authors.initials: Q
authors.lastname: Shao
authors.forename: Wenjuan
authors.initials: W
authors.lastname: Gao
authors.forename: Bingfeng
authors.initials: B
authors.lastname: Song
authors.forename: Lei
authors.initials: L
authors.lastname: Wang
authors.forename: Xiaobin
authors.initials: X
authors.lastname: Song
authors.forename: Xun
authors.initials: X
authors.lastname: Qu
authors.forename: Fengcai
authors.initials: F
authors.lastname: Wei
mesh_terms: D017209:Apoptosis; D002294:Carcinoma, Squamous Cell / Q000378:metabolism / Q000473:pathology; D045744:Cell Line, Tumor; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D016547:Kinesins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D009062:Mouth Neoplasms / Q000378:metabolism / Q000473:pathology; D019869:Phosphatidylinositol 3-Kinases / Q000235:genetics / Q000378:metabolism*; D000081082:Phosphoinositide-3 Kinase Inhibitors; D051057:Proto-Oncogene Proteins c-akt / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D034622:RNA Interference; D012333:RNA, Messenger / Q000378:metabolism; D034741:RNA, Small Interfering / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D007334:Insulin-Like Growth Factor I; D016547:Kinesins; D019869:Phosphatidylinositol 3-Kinases; D000081082:Phosphoinositide-3 Kinase Inhibitors; D051057:Proto-Oncogene Proteins c-akt; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D034741:RNA, Small Interfering; C509805:KIF2A protein, human