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Supplemental Digital Content is available in the text.MicroRNAs (miRNAs) have been documented as critical regulators in ischemia/reperfusion-induced neuronal death. A better understanding of miRNA-mediated molecular mechanisms in ischemia/reperfusion-induced neuronal death may provide therapeutic targets for cerebral ischemia/reperfusion injury. A growing body of evidence suggests that miR-429 is a apoptosis-related miRNA that is also induced by hypoxia. However, whether miR-429 is involved in regulating neuronal apoptosis during cerebral ischemia/reperfusion injury remains unclear. In this study, the effect of miR-429 on oxygen–glucose deprivation and reoxygenation (OGD/R)-induced neuronal injury was investigated in vitro. The results showed that miR-429 expression levels were upregulated in cultured neurons with OGD/R treatment. The downregulation of miR-429 significantly alleviated OGD/R-induced neuronal injury, whereas upregulation of miR-429 aggravated it. Bioinformatic analysis showed that miR-429 could directly target the 3′-untranslated region of GATA-binding protein 4 (GATA4), which was verified by dual-luciferase reporter assay. Moreover, we found that miR-429 negatively regulated GATA4 expression. Overexpression of GATA4 also significantly alleviated OGD/R-induced neuronal injury. However, knockdown of GATA4 partially reversed the protective effect induced by miR-429 downregulation. Overall, our data showed that downregulation of miR-429 protected neurons against OGD/R-induced injury by promoting GATA4 and suggested a potential therapeutic target for the treatment of cerebral ischemia/reperfusion injury.

Esophageal squamous cell carcinoma (ESCC) is a malignancy of the alimentary tract resulting in death worldwide. The role and underlying mechanism of hsa-miR-1269a in the progression of ESCC remain unclear. In this study, hsa-miR-1269a was screened by differential expression analysis in TCGA, and its target gene FAM46C was predicted. qRT-PCR was conducted to assay the expression of hsa-miR-1269a and FAM46C in ESCC cells. The results showed that hsa-miR-1269a was upregulated in ESCC tissues and cell lines. Hsa-miR-1269a overexpression stimulated the proliferation, migration, and invasion capacities of ESCC cells, and FAM46C overexpression inhibited these phenotypes. Dual-luciferase assay verified that hsa-miR-1269a could target FAM46C. Next, qRT-PCR and western blot demonstrated that hsa-miR-1269a overexpression downregulated FAM46C. Rescue experiments revealed that hsa-miR-1269a accelerated the malignant progression of ESCC through FAM46C down-regulation. These results indicate that the interaction between hsa-miR-1269a and FAM46C plays a regulatory role in driving the malignant progression of ESCC cells, thereby providing a novel molecular mechanism for understanding ESCC.