Inhibition of GSK 3β Activity Is Associated with Excessive EZH2 Expression and Enhanced Tumour Invasion in Nasopharyngeal Carcinoma

• DOI: 10.1371/journal.pone.0068614
• Publication Date: 2013-07-18T22:54:32Z
• Authors: Renqiang Ma; Yi Wei; Xiaoming Huang; Ran Fu; Xi Luo; Xiaolin Zhu; Wenbin Lei; Jugao Fang; Huabin Li; Weiping Wen
• Keywords: Immunoprecipitation

Background Enhancer of zeste homolog 2 (EZH2) has been shown to contribute tumour development and/or progression. However, the signalling pathway underlying regulation EZH2 in nasopharyngeal carcinoma (NPC) remains unclear. Since contains putative Glycogen synthase kinase 3 beta (GSK3β) phosphorylation motif ADHWDSKNVSCKNC (591) and may act as a possible substrate GSK-3β, it is that inactivation GSK3β lead excessive expression NPC. Method We first examined phosphorylated (p-GSK3β) by immunohistochemical staining NPC samples. Then, we evaluated interaction using immunoprecipitation immune blot. Moreover, determined effect inhibition activity on tumor invasiveness cell lines vitro. Finally, invasive properties cells after knocking down with siRNA. Results found correlated at Ser 9 (an inactivated form GSK3β) human also provided evidence able interact Furthermore, can upregulation vitro, enhanced local invasiveness. By siRNA, these were dependent. Conclusion Our findings indicate account for overexpression subsequent progression, this mechanism might be potential target therapy.