当前位置: X-MOL 学术Pathol. Oncol. Res. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Overexpression of Long Non-Coding RNA FGF14-AS2 Inhibits Colorectal Cancer Proliferation Via the RERG/Ras/ERK Signaling by Sponging microRNA-1288-3p.
Pathology & Oncology Research ( IF 2.8 ) Pub Date : 2020-07-11 , DOI: 10.1007/s12253-020-00862-8
Ruizhi Hou 1 , Yan Liu 2 , Yanzhuo Su 1 , Zhenbo Shu 1
Affiliation  

Colorectal cancer remains one of most common cancer types with poor prognosis globally. Recent years, numerous studies depicted pivotal roles of lncRNAs in colorectal cancer progression. This study aimed to investigate the role of FGF14-AS2 in colorectal cancer development. FGF14-AS2 was found as a significantly downregulated lncRNA in TCGA dataset. Via RT-qPCR, we confirmed the downregulation of FGF14-AS2 in collected colorectal carcinoma samples. Transfection of plasmid containing full length of FGF14-AS2 repressed cell proliferation and induced elevation of cell apoptosis in colorectal cancer cells. In addition, FGF14-AS2 overexpression inactivated MAPK/ERK signaling in cells. Bioinformatic analysis and subsequent cell-based assays showed that FGF14-AS2 sponging miR-1288-3p, an oncogenic miRNA in colorectal cancer. RERG, the regulator of Ras/ERK pathway, was predicted and verified as target gene of miR-1288. Via downregulation of miR-1288, FGF14-AS2 elevated RERG expression in colorectal cancer cells. Rescue assays indicated that FGF14-AS2 relied on regulation of RERG to control cell proliferation and apoptosis in colorectal cancer. Taken together, the current study demonstrated FGF14-AS2 as a regulator of colorectal cancer development via downregulation of miR-1288-3p and inactivation of Ras/ERK signaling.



中文翻译:

长的非编码RNA FGF14-AS2的过表达通过将microRNA-1288-3p海绵化,通过RERG / Ras / ERK信号抑制大肠癌的增殖。

大肠癌仍然是全球最常见的预后不良的癌症之一。近年来,许多研究描述了lncRNA在大肠癌进展中的关键作用。这项研究旨在调查FGF14-AS2在结直肠癌发展中的作用。在TCGA数据集中发现FGF14-AS2是显着下调的lncRNA。通过RT-qPCR,我们确认了收集的大肠癌样品中FGF14-AS2的下调。含有全长FGF14-AS2的质粒的转染抑制了结直肠癌细胞的细胞增殖并诱导了细胞凋亡的升高。另外,FGF14-AS2过表达使细胞中的MAPK / ERK信号失活。生物信息学分析和随后的基于细胞的分析表明,FGF14-AS2使miR-1288-3p海绵化,这是大肠癌中的致癌miRNA。RERG,Ras / ERK通路的调节剂被预测并证实是miR-1288的靶基因。通过下调miR-1288,FGF14-AS2可提高结直肠癌细胞中的RERG表达。救援试验表明,FGF14-AS2依赖于RERG的调控来控制结直肠癌的细胞增殖和凋亡。综上所述,当前的研究表明,FGF14-AS2通过下调miR-1288-3p和灭活Ras / ERK信号传导,成为大肠癌发展的调节剂。

更新日期:2020-07-13
down
wechat
bug