竞争性内源性RNA
基因敲除
癌症研究
细胞生长
癌变
长非编码RNA
生物
下调和上调
小RNA
免疫印迹
骨肉瘤
细胞迁移
转移
分子生物学
细胞
癌症
细胞培养
基因
遗传学
作者
Hongkai Lian,Panpan Xie,Ningwei Yin,Jingyi Zhang,Xinan Zhang,Jing Li,Chunyan Zhang
出处
期刊:Life Sciences
[Elsevier]
日期:2019-09-01
卷期号:233: 116757-116757
被引量:31
标识
DOI:10.1016/j.lfs.2019.116757
摘要
Previous studies have demonstrated that long non-coding RNAs (lncRNAs) were involved in tumorigenesis in various human neoplasms, including osteosarcoma (OS). However, the expression and specific role of lncRNA linc00460 in OS remain unknown. Bioinformatics analysis, Quantitative real-time polymerase chain reaction (qRT-PCR), CCK-8 assay, Colony formation assay, Wound healing assay, Transwell assay, Dual luciferase reporter assay, RNA immunoprecipitation and Western blot were utilized to analyze or detect survival, gene expression, cell proliferation, cell migration, cell invasion and interest protein levels, respectively. In this study, we found high linc00460 expression predicted poor prognosis of pan-cancer patients. Linc00460 was up-regulated in OS tissues and cells. High linc00460 expression was positively correlated with distant metastasis and poor overall survival of OS patients. Knockdown of linc00460 suppressed OS cells proliferation and metastasis in vitro. In addition, an inverse correlation between linc00460/miR-1224-5p and miR-1224-5p/FADS1 was observed in OS. Mechanistically, linc00460 functioned as a competitively endogenous RNA (ceRNA) to up-regulate FADS1 expression via sponging miR-1224-5p in OS, thereby promoting OS progression. In conclusion, this study recognized linc00460 as a new oncogenic lncRNA in OS and suggests that the linc00460/miR-1224-5p/FADS1 axis might be a potential therapeutic target for OS.
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