Παρασκευή 30 Σεπτεμβρίου 2016

KAI1 Overexpression Promotes Apoptosis and Inhibits Proliferation, Cell Cycle, Migration, and Invasion in Nasopharyngeal Carcinoma cells

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Publication date: Available online 28 September 2016
Source:American Journal of Otolaryngology
Author(s): Zheng Guo, Yili Wang, Jing Yang, Jinghua Zhong, Xia Liu, Mingjun Xu
ObjectivesThe purpose of this study is to characterize the effect of KAI1 Overexpression on the biological behaviour of nasopharyngeal carcinoma (NPC) cells.BackgroundNasopharyngeal carcinoma is a highly malignant tumor with a high rate of incidence in China. Currently, there are no ideal therapeutic options for patients with NPC, but a targeted therapy would have great potential for treating it. Therefore, there is an urgent need for novel therapeutic targets to provide new options for treating NPC. The KAI1 gene was originally identified as a metastasis suppressor gene for advanced human cancer. In NPC cell lines and tissues, the expression of KAI1 decreased as the metastatic potential of cells increased, but its potential as a therapeutic target has not been elucidated.MethodsNon-transformed nasopharyngeal epithelium cell NP69 and NPC cell line C666–1 were cultured and KAI1 expression in these cells was detected by qRT-PCR and western blot. After the transfection of KAI1-pCDNA3.1 to NP69 and C666–1, the KAI1 expression in these cells was detected by qRT-PCR and western blot, the proliferation was performed by MTS, the cell cycle and apoptosis were performed by flow cytometry, the migration and invasion were examined by transwell.ResultsOur results showed that KAI1 was significantly upregulated in C666–1 cells compared to that in NP69 cells. In addition, KAI1 overexpression significantly inhibited the proliferation, cell cycle, migration, and invasion, and promoted apoptosis of C666–1 cells, but had no significant effect on NP69 cells.ConclusionOur findings suggest that KAI1 overexpression promotes apoptosis and inhibits proliferation, cell cycle, migration, and invasion in NPC cells. We hypothesize that KAI1 overexpression could be a potential therapeutic target for NPC.



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