MiR-24 functions as a tumor suppressor in nasopharyngeal carcinoma through targeting FSCN1.
BACKGROUND
Increasing evidence indicates that the dysregulation of miRNAs expression is involved in the tumorigenesis by acting as tumor suppressors or oncogenes. However, no study investigates the function and mechanisms of miR-24 in nasopharyngeal carcinoma (NPC).


METHODS
Quantitative RT-PCR, MTT, colony formation, soft-agar, wound healing, Transwell migration and invasion assays, and xenograft tumor growth and lung metastasis models were performed to test the expression levels and functions of miR-24 in NPC. Luciferase reporter assay, quantitative RT-PCR, Western blotting, and immunohistochemistry were used to identify and verify the target of miR-24.


RESULTS
The results showed that MiR-24 was obviously downregulated in NPC cell lines and tissue samples (P < 0.05). Ectopic expression of miR-24 inhibited the cell viability, proliferation, migration, and invasion in vitro (all P < 0.05), and suppressed the xenograft tumor growth and lung metastasis formation in vivo (all P < 0.05). Fascin homologue 1 (FSCN1) was verified as a direct target of miR-24, and silencing FSCN1 expression with small interfering RNA inhibited NPC cell proliferation and invasion (all P < 0.05).


CONCLUSIONS
Overall, miR-24 acts as a novel tumor suppressor in the development and progression of NPC through targeting FSCN1, which providing new insight into the mechanisms of NPC carcinogenesis and suggesting the possibility of miR-24 as a therapeutic target.
Guangzhou First People's hospital, Guangzhou Medical University, 1 Panfu Road, Guangzhou, Guangdong, 510180, PR China. hare0914@gzhmu.edu.cn.
Ying-Qing
YQ
Li
Guangzhou First People's hospital, Guangzhou Medical University, 1 Panfu Road, Guangzhou, Guangdong, 510180, PR China.
Jian-Hua
JH
Lu
Guangzhou First People's hospital, Guangzhou Medical University, 1 Panfu Road, Guangzhou, Guangdong, 510180, PR China.
Xue-Ming
XM
Bao
Guangzhou First People's hospital, Guangzhou Medical University, 1 Panfu Road, Guangzhou, Guangdong, 510180, PR China.
Xi-Fu
XF
Wang
Guangzhou First People's hospital, Guangzhou Medical University, 1 Panfu Road, Guangzhou, Guangdong, 510180, PR China.
Jun-Hua
JH
Wu
Guangzhou First People's hospital, Guangzhou Medical University, 1 Panfu Road, Guangzhou, Guangdong, 510180, PR China.
Wei-Qiang
WQ
Hong
D000818:Animals; D001483:Base Sequence; D001665:Binding Sites; D002277:Carcinoma; D002352:Carrier Proteins / Q000235:genetics*; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics; D049109:Cell Proliferation; D004195:Disease Models, Animal; D015536:Down-Regulation; D015972:Gene Expression Regulation, Neoplastic; D016147:Genes, Tumor Suppressor; D064593:Heterografts; D006801:Humans; D008297:Male; D051379:Mice; D035683:MicroRNAs / Q000737:chemistry / Q000235:genetics*; D008840:Microfilament Proteins / Q000235:genetics*; D000077274:Nasopharyngeal Carcinoma; D009303:Nasopharyngeal Neoplasms / Q000235:genetics* / Q000473:pathology; D009362:Neoplasm Metastasis; D034622:RNA Interference; D012333:RNA, Messenger / Q000737:chemistry / Q000235:genetics; D047368:Tumor Burden / Q000235:genetics
D002352:Carrier Proteins; C502658:FSCN1 protein, human; C543845:MIRN24 microRNA, human; D035683:MicroRNAs; D008840:Microfilament Proteins; D012333:RNA, Messenger