Oncotarget

Research Papers:

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

Qingmei He, Xianyue Ren, Jiewei Chen, Yingqin Li, Xinran Tang, Xin Wen, Xiaojing Yang, Jian Zhang, Yaqin Wang, Jun Ma and Na Liu _

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Oncotarget. 2016; 7:3047-3058. https://doi.org/10.18632/oncotarget.6504

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Abstract

Qingmei He1,*, Xianyue Ren1,*, Jiewei Chen1,*, Yingqin Li1, Xinran Tang1, Xin Wen1, Xiaojing Yang1, Jian Zhang1, Yaqin Wang1, Jun Ma1, Na Liu1

1Sun Yat-Sen University Cancer Center, State Key laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, People’s Republic of China

*These authors contributed equally to this work

Correspondence to:

Na 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, 2015     Published: December 08, 2015

ABSTRACT

Dysregulation of miRNAs has been shown to contribute to the carcinogenesis and progression of nasopharyngeal carcinoma (NPC). Our previous microarray data showed that miR-16 expression is significantly decreased in archived NPC tissues. Here, we confirmed that miR-16 was reduced in NPC cell lines and freshly-frozen samples. Ectopic expression of miR-16 suppressed NPC cell proliferation, migration, and invasion in vitro and inhibited tumor growth and metastatic colonization in the lung in vivo. Furthermore, fibroblast growth factor 2 (FGF2) was identified as a direct target of miR-16, and both phosphoinositide-3- kinase/AKT (PI3K/AKT) and mitogen-activated protein kinase (MAPK) signaling pathways were repressed after miR-16 overexpression. In addition, the restoration of FGF2 reversed the suppressive effects of miR-16. Together, these results indicated that miR-16 suppresses NPC carcinogenesis and progression by targeting FGF2, thereby representing a potential target for miRNA-based therapy for NPC in the future.


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