lncRNA ROR1-AS1 Regulates the Proliferation, Migration, Invasion and Apoptosis of Neuroblastoma Cells SK-N-SH by Targeting miR-758-3p
The purpose of this study was to explore the effect and mechanism of ROR1-AS1 on the proliferation, migration, invasion and apoptosis of neuroblastoma cells SK-N-SH. Sixty-seven cases of neuroblastoma tissue and adjacent tissues were collected, and RT-qPCR was used to detect the expression levels of ROR1-AS1 and miR-758-3p in the tissues. ROR1-AS1 small interfering RNA or miR-758-3p mimics were transfected into SK-N-SH cells, or ROR1-AS1 small interfering RNA and miR-758-3p inhibitor were co-transfected into SK-N-SH cells. CCK-8 method was used to detect cell proliferation. Transwell was used to detect cell migration and invasion. Flow cytometry was used to detect cell apoptosis, and Western blot was used to detect the protein expression levels of CyclinD1, p21, Bcl-2, Bax, MMP-2 and MMP-9. The dual luciferase reporter gene experiment verified the regulatory relationship between ROR1-AS1 and miR-758-3p. The results showed that the expression of ROR1-AS1 in neuroblastoma tissues was higher than that in adjacent tissues, but the expression of miR-758-3p was lower than that in adjacent tissues. Inhibiting ROR1-AS1 or overexpressing miR-758-3p reduced the activity of SK-N-SH cells, the number of migrating cells, the number of invasion cells, as well as the protein expression of CyclinD1, Bcl-2, MMP-2 and MMP-9 in cells. But inhibiting ROR1-AS1 or overexpressing miR-758-3p increased the apoptosis rate of SK-N-SH cells and the protein expression of p21 and Bax in cells. ROR1-AS1 negatively regulated the expression of miR-758-3p in SK-N-SH cells. Interfering with miR-758-3p reversed the effect of inhibiting ROR1-AS1 on proliferation, migration, invasion and apoptosis of SK-N-SH cells. This suggested that inhibiting ROR1-AS1 might block the proliferation, migration and invasion of SK-N-SH cells and promote cell apoptosis by targeting to up-regulate the expression of miR-758-3p. ROR1-AS1 may become a molecular target for neuroblastoma treatment.
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