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

被引：61

作者：

He, Qingmei ^{[1
]}

Ren, Xianyue ^{[1
]}

Chen, Jiewei ^{[1
]}

Li, Yingqin ^{[1
]}

Tang, Xinran ^{[1
]}

Wen, Xin ^{[1
]}

Yang, Xiaojing ^{[1
]}

Zhang, Jian ^{[1
]}

Wang, Yaqin ^{[1
]}

Ma, Jun ^{[1
]}

Liu, Na ^{[1
]}

机构：

[1] Sun Yat Sen Univ, Ctr Canc, State Key Lab Oncol South China, Collaborat Innovat Ctr Canc Med, Guangzhou 510275, Guangdong, Peoples R China

来源：

ONCOTARGET | 2016年 / 7卷 / 03期

基金：

中国国家自然科学基金;

关键词：

miR-16; fibroblast growth factor 2; nasopharyngeal carcinoma; tumor growth; metastasis; NASOPHARYNGEAL CARCINOMA; LUNG-CANCER; TUMOR ANGIOGENESIS; PROGNOSTIC VALUE; DOWN-REGULATION; POOR-PROGNOSIS; METASTASIS; EXPRESSION; SUPPRESSES; FGF2;

D O I：

10.18632/oncotarget.6504

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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.

引用

页码：3047 / 3058

页数：12

共 46 条

[1] miR-15a and miR-16-1 in cancer: discovery, function and future perspectives [J].