基因敲除
骨肉瘤
癌症研究
亚细胞定位
小RNA
长非编码RNA
核糖核酸
荧光原位杂交
原位杂交
竞争性内源性RNA
肿瘤进展
生物
细胞质
分子生物学
化学
细胞生物学
信使核糖核酸
基因
遗传学
染色体
作者
Farui Sun,Ziliang Yu,Bingbing Wu,Haiping Zhang,Jing Ruan
摘要
Abstract Background Numerous studies have shown that aberrant expression of long non‐coding RNAs (lncRNAs) is associated with the development and metastasis of osteosarcoma (OS). However, the role and function of LINC00319 with respect to regulating OS progression is unknown. The present study aimed to reveal the function and related mechanism of LINC00319 in OS. Methods The expression of LINC00319, miR‐455‐3p and nuclear factor IB (NFIB) in OS cells and tissues was determined using a reverse transcriptase‐polymerase chain reaction (PCR). The sublocalization of LINC00319 was predicted by the lncATLAS database ( http://lncatlas.crg.eu ) and RNA fluorescence in situ hybridization (FISH) was further performed to detect the subcellular localization of LINC00319. LINC00319, miR‐455‐3p and NFIB target sites were predicted by StarBase ( http://starbase.sysu.edu.cn/index.php ) and validated using a dual luciferase reporter gene assay. We subsequently performed LINC00319 gain‐ and loss‐of‐function studies to define the role of LINC00319 in OS cell migration. Results PCR results showed that lncRNA LINC00319 exhibited high expression in tumor cells and tissue. Moreover, LINC00319 was positioned in the cytoplasm, which was identified by FISH. Knockdown of lncRNA LINC00319/NFIB or overexpression of miR‐455‐3p blocked the migration of OS cells. In addition, the inhibitory effect of migration with the knockdown of lncRNA LINC00319 was partially blocked by administration of miR‐455‐3p inhibitor. Conclusions lncRNA LINC00319 may promote OS progression by regulating the miR‐455‐3p/NFIB axis, which probably serves as an innovative potential indicator of prognosis and a target of therapy for OS.
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