Abstract
BACKGROUND: Long non-coding RNAs (lnc-RNAs) and microRNAs (miRNAs) play key roles in the development of stroke. However, the role of lncRNA FTX in stroke is limited known. METHODS: Real-time polymerase chain reaction (real-time PCR) assays were used to measure the expression of lncRNA FTX, miR-342-3p and SPI1. Western blot assays were employed to examine SPI1 protein expression. The cell viability was measured by CCk8 assay. Cell migration was detected by wound healing assays and transwell assays. Angiogenesis was evaluated by matrigel tube formation assays. The interaction between lncRNA FTX, miR-342-3p and SPI1 was confirmed by site-directed mutagenesis and luciferase assays. RESULTS: The expression of lncRNA FTX was down-regulated in blood sample from stroke patients, MAO mice tissues and OGD/R treated BMECs. Overexpression of lncRNA FTX could increase the cell viability, migration and angiogenesis in OGD/R treated BMECs. LncRNA FTX could act as a ceRNA for miR-342-3p. Furthermore, miR-342-3p inhibition increased migration and angiogenesis in OGD/R-induced BMECs. Dual-luciferase reporter assay verified that SPI1 was a target of miR-342-3p. CONCLUSION: In summary, lncRNA FTX enhanced the angiogenesis in stroke by acting as a sponge of miR-342-3p to regulate the expression of SPI1 level.