Long intergenic non-protein coding RNA 115 (LINC00115) aggravates retinoblastoma progression by targeting microRNA miR-489-3p that downregulates 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 2 (PFKFB2)

长链非蛋白质编码RNA 115 (LINC00115) 通过靶向下调6-磷酸果糖-2-激酶/果糖-2,6-二磷酸酶2 (PFKFB2) 的microRNA miR-489-3p 加剧视网膜母细胞瘤的进展。

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Abstract

Long non-coding RNAs (lncRNAs) are key regulators of cancer. However, the role of long intergenic non-protein coding RNA 115 (LINC00115) in the regulation of retinoblastoma (RB) has not yet been studied. The expression levels of LINC00115, microRNA (miR)-489-3p, and 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 2 (PFKFB2) in RB tissues or cells were detected by quantitative reverse transcription-polymerase chain reaction. The proliferation and migration of cells were detected by the cell counting kit-8 and Transwell assays. Luciferase reporter gene analysis and RNA immunoprecipitation assay were used to validate the target gene interactions predicted by starBase. A xenograft tumor experiment was conducted to validate the in vivo outcomes. The expression levels of LINC00115 and PFKFB2 in RB tissues were higher than those in normal tissues, while miR-489-3p showed the opposite trend. Silencing of LINC00115 inhibited the proliferation and migration of SO-RB50 and HXO-RB44 cells. An inhibitory or facilitated effect on RB tumorigenesis was observed following PFKFB2 silencing or miR-489-3p overexpression, respectively. Moreover, LINC00115 aggravated RB progression by targeting miR-489-3p, which downregulated PFKFB2. This finding improves our understanding of the relationship between LINC00115 and RB. Furthermore, miR-489-3p and PFKFB2 may be used as potential targets for RB prevention and treatment.

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