Background Long non-coding RNA (lncRNA) small nucleolar RNA host gene 14 (SNHG14) is associated with cerebral ischemia–reperfusion (CI/R) injury. This work aims to explore the role of SNHG14 in CI/R injury. Methods HT22 (mouse hippocampal neuronal cells) cell model was established by oxygen–glucose deprivation/reoxygenation (OGD/R) treatment. The interaction among SNHG14, miR-182-5p and BNIP3 was verified by luciferase reporter assay. Flow cytometry, western blot and quantitative real-time PCR were performed to examine apoptosis, the expression of genes and proteins. Results SNHG14 and BNIP3 were highly expressed, and miR-182-5p was down-regulated in the OGD/R-induced HT22 cells. OGD/R-induced HT22 cells exhibited an increase in apoptosis. SNHG14 overexpression promoted apoptosis and the expression of cleaved-caspase-3 and cleaved-caspase-9 in the OGD/R-induced HT22 cells. Moreover, SNHG14 up-regulation enhanced the expression of BNIP3, Beclin-1, and LC3II/LC3I in the OGD/R-induced HT22 cells. Furthermore, SNHG14 regulated BNIP3 expression by sponging miR-182-5p. MiR-182-5p overexpression or BNIP3 knockdown repressed apoptosis in OGD/R-induced HT22 cells, which was abolished by SNHG14 up-regulation. Conclusion Our study demonstrates that lncRNA SNHG14 promotes OGD/R-induced neuron injury by inducing excessive mitophagy via miR-182-5p/BINP3 axis in HT22 mouse hippocampal neuronal cells. Thus, SNHG14/miR-182-5p/BINP3 axis may be a valuable target for CI/R injury therapies.

Various studies have manifested that microRNAs (miRNAs) are involved in the modulation of the occurrence and development of osteosarcoma (OS). However, whether miR-22-3p is associated with OS growth remains unclear. In the study, the potential molecular mechanisms of miR-22-3p in OS was explored. It was affirmed that miR-22-3p was associated with distant metastasis and tumor size in OS patients, and reduced in OS tissues and cells while transcription factor 7-like 2 (TCF7L2) was elevated. Elevated miR-22-3p repressed OS cell progression, and the Wnt/β-catenin pathway, while elevated TCF7L2 was opposite. MiR-22-3p targeted TCF7L2 in OS. In functional rescue experiments, knockdown of miR-22-3p on OS progression and promotion of Wnt/β-catenin were reversed by simultaneous knockdown of TCF7L2. Transplantation experiments in nude mice showed that elevated miR-22-3p repressed OS tumor growth and decreased TCF7L2, Wnt and β-catenin. Shortly, this study suggest that miR-22-3p refrains the Wnt/β-catenin pathway by targeting TCF7L2 and thereby preventing OS deterioration. MiR-22-3p/TCF7L2 axis is supposed to be a candidate molecular target for future OS treatment.

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