Flotillin-2 promotes metastasis of nasopharyngeal carcinoma by activating NF-κB and PI3K/Akt3 signaling pathways

• DOI: 10.1038/srep11614
• Publication Date: 2015-07-24T09:09:47Z
• Authors: Jie Liu; Wei Huang; Caiping Ren; Qiuyuan Wen; Weidong Liu; Xuyu Yang; Lei Wang; Bin Zhu; Liang Zeng; Xiangling Feng; Chang Zhang; Huan Chen; Wei Jia; Lihua Zhang; Xiaomeng Xia; Yuxiang Chen
• Keywords: 0301 basic medicine; Nasopharyngeal Carcinoma; Carcinoma; NF-kappa B; Membrane Proteins; Mice, Nude; Nasopharyngeal Neoplasms; Article; 3. Good health; Mice; Phosphatidylinositol 3-Kinases; 03 medical and health sciences; Cell Line, Tumor; Animals; Heterografts; Humans; Neoplasm Metastasis; Proto-Oncogene Proteins c-akt; Neoplasm Transplantation; Signal Transduction

Abstract Lipid raft proteins have been confirmed to be important in cell signal transduction. Some reports shown that the aberrant expression of lipid is associated with malignant phenotypes some cancers. However, role protein flotillin-2 (Flot-2) nasopharyngeal carcinoma (NPC) remains comprehensively characterized. Here, overexpression Flot-2 NPC tissues and lines was detected by immunostaining found positively metastasis. Furthermore, inhibiting impaired malignancy highly metastatic line 5-8F constraining its growth proliferation, mobility migration decreasing capacity cells metastasize nude mice. In contrast, forced increased 6-10B, a non-metastatic weakly expresses Flot-2. Moreover, 5-8F-shFlot-2 cells, which inhibited expression, NF-κB PI3K/Akt3 pathways were inactivated. Subsequently, MMPs decreased Foxo1 activity increased. addition, enhanced activities observed overexpressing 6-10B cells. Thus, exerts pro-neoplastic involved tumor progression through signaling.