miR-100 Inhibits Cell Growth and Proliferation by Targeting HOXA1 in Nasopharyngeal Carcinoma

被引:17
|
作者
He, Weifeng [1 ]
Huang, Yun [2 ]
Jiang, Cheng Chuan [1 ]
Zhu, Yuan [3 ]
Wang, Ling [4 ]
Zhang, Weiwei [1 ]
Huang, Weiguo [2 ]
Zhou, Ting [1 ,5 ]
Tang, Sanyuan [1 ]
机构
[1] Brain Hosp Hunan Prov, Dept Oncol, Changsha 410007, Hunan, Peoples R China
[2] Univ South China, Hengyang Med Coll, Canc Res Inst, Hengyang 421001, Hunan, Peoples R China
[3] Peoples Hosp Changshou Chongqing, Chongqing 401220, Peoples R China
[4] Yi Chang Cent Peoples Hosp, Yichang 443000, Hubei, Peoples R China
[5] Hunan Univ Tradit Chinese Med, Coll Pharm, Dept Clin Pharm, Changsha 410007, Hunan, Peoples R China
来源
ONCOTARGETS AND THERAPY | 2020年 / 13卷
关键词
miR-100; nasopharyngeal carcinoma; proliferation; invasion; HOXA1; HEPATOCELLULAR-CARCINOMA; DOWN-REGULATION; CANCER-CELLS; MICRORNA-100; INVASION; METASTASIS; EXPRESSION; SUPPRESSES; SURVIVAL; DEREGULATION;
D O I
10.2147/OTT.S228783
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Background: Increasing evidence indicates that the dysregulation of miRNAs plays a vital role in tumorigenesis and progression of nasopharyngeal carcinoma (NPC). Thus, it is necessary to further investigate the function and mechanism of miRNAs in NPC. Methods: miR-100 expression was analyzed using publicly available databases and then tested using quantitative RT-PCR in NPC tissues and cell lines. MTT and colony formation assays and xenograft tumor model were used to test the NPC cell growth and proliferation abilities while modulating miR-100 expression. The target of miR-100 was predicted with TargetScan and validated with luciferase reporter assay, quantitative RT-PCR, and Western blot. Results: The expression of miR-100 was significantly reduced in NPC tissues and cell lines. Overexpression of miR-100 obviously suppressed NPC cell growth and proliferation, whereas silencing miR-100 promoted NPC cell growth and proliferation in vitro. HOXA1 (homeobox A1) was validated as a direct target of miR-100, and restoring HOXA1 expression could reverse the inhibitive effect of miR-100 on NPC cell growth and proliferation. The mRNA and protein expression of HOXA1 was increased in NPC cell lines. Furthermore, ectopic expression of miR-100 inhibited xenograft tumor growth in vivo. Conclusion: Taken together, our findings suggest that miR-100 could suppress NPC growth and proliferation through targeting HOXA1, providing a novel target for the miRNA-mediated therapy for patients with NPC in the future.
引用
收藏
页码:593 / 602
页数:10
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