LINC00319 promotes osteosarcoma progression by regulating the miR-455-3p/NFIB axis.

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. 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. 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. 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.

Sun F ，Yu Z ，Wu B ，Zhang H ，Ruan J ... -  《-》

Long Non-Coding RNA TUG1 Promotes Proliferation and Inhibits Apoptosis of Osteosarcoma Cells by Sponging miR-132-3p and Upregulating SOX4 Expression.

Li G ，Liu K ，Du X 《-》

Linc00460 promotes osteosarcoma progression via miR-1224-5p/FADS1 axis.

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.

Lian H ，Xie P ，Yin N ，Zhang J ，Zhang X ，Li J ，Zhang C ... -  《-》

LncRNA MIAT facilitates osteosarcoma progression by regulating mir-128-3p/VEGFC axis.

The aberrant expression of long non-coding RNAs (lncRNAs) has been involved in the progression of many human tumors including osteosarcoma (OS). However, the biological function and the underlying mechanism of the lncRNA myocardial infarction-associated transcript (MIAT) in OS remain unclear. In the present study, we found that lncRNA MIAT was significantly up-regulated in both OS tissues and cell lines, and high expression of MIAT was positively associated with tumor size and lymph node metastasis of OS patients. In addition, knockdown of MIAT inhibited proliferation, migration, invasion and promoted apoptosis of OS cells in vitro. Moreover, the expression of MIAT was negatively associated with miR-128-3p but positively correlated with vascular endothelial growth factor C (VEGFC) in OS. Further mechanistic study revealed that lncRNA MIAT promoted OS progression by up-regulating VEGFC via sponging miR-128-3p in vitro. Taken together, our results suggest that MIAT/miR-128-3p/VEGFC axis contributes to OS progression and may be used as a novel therapeutic target for OS. © 2019 IUBMB Life, 9999(9999):1-9, 2019.

Zhang C ，Xie L ，Liang H ，Cui Y ... -  《-》

Long noncoding RNA CRNDE functions as a diagnostic and prognostic biomarker in osteosarcoma, as well as promotes its progression via inhibition of miR-335-3p.

Yu Y ，Wang L ，Li Z ，Zheng Y ，Shi Z ，Wang G ... -  《-》