miR-16 targets fibroblast growth factor 2 to inhibit NPC cell proliferation and invasion via PI3K/AKT and MAPK signaling pathways

0301 basic medicine Mice, Inbred BALB C 0303 health sciences Lung Neoplasms Nasopharyngeal Carcinoma Carcinogenesis MAP Kinase Signaling System Carcinoma Mice, Nude Nasopharyngeal Neoplasms Genetic Therapy 3. Good health Gene Expression Regulation, Neoplastic Mice MicroRNAs 03 medical and health sciences Cell Line, Tumor Disease Progression Animals Humans Fibroblast Growth Factor 2 Neoplasm Invasiveness Mitogen-Activated Protein Kinases Research Paper Cell Proliferation
DOI: 10.18632/oncotarget.6504 Publication Date: 2015-12-09T05:12:28Z
ABSTRACT
// Qingmei He 1, * , Xianyue Ren Jiewei Chen Yingqin Li 1 Xinran Tang Xin Wen Xiaojing Yang Jian Zhang Yaqin Wang Jun Ma Na Liu Sun Yat-Sen University Cancer Center, State Key laboratory of Oncology in South China, Collaborative Innovation Center Medicine, Guangzhou, People’s Republic China These authors contributed equally to this work Correspondence to: Liu, e-mail: liun1@sysucc.org.cn Keywords: miR-16, fibroblast growth factor 2, nasopharyngeal carcinoma, tumor growth, metastasis Received: August 13, 2015      Accepted: November 21, Published: December 08, 2015 ABSTRACT Dysregulation miRNAs has been shown contribute the carcinogenesis and progression carcinoma (NPC). Our previous microarray data showed that miR-16 expression is significantly decreased archived NPC tissues. Here, we confirmed was reduced cell lines freshly-frozen samples. Ectopic suppressed proliferation, migration, invasion vitro inhibited metastatic colonization lung vivo . Furthermore, 2 ( FGF2 ) identified as a direct target both phosphoinositide-3- kinase/AKT PI3K/AKT mitogen-activated protein kinase MAPK signaling pathways were repressed after overexpression. In addition, restoration reversed suppressive effects miR-16. Together, these results indicated suppresses by targeting thereby representing potential for miRNA-based therapy future.
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