Background: MicroRNA-1269 (miR-1269) has been identified upregulated in several cancers, as well as in esophageal cancer. In the present study, we investigated the clinical prognostic significance and potential functional role of miR-1269 in esophageal squamous cell carcinoma (ESCC). Methods: A total of 107 ESCC patients who underwent surgical resection were enrolled in this study. miR-1269 expression was measured using quantitative real-time PCR (qRT-PCR). Kaplan-Meier method and multivariate Cox regression analysis were used to explore the prognostic significance of miR-1269. CCK-8 assays and Transwell assays were used to investigate the effects of miR-1269 on cell proliferation, migration, and invasion. The direct association between miR-1269 and SOX6 was evaluated using a dual-luciferase reporter assay. Results: The expression of miR-1269 was significantly upregulated in ESCC tissues and cell lines compared with adjacent normal tissues and esophageal epithelial cell line, respectively. What’s more, the upregulation of miR-1269 was associated with positive lymph node metastasis and advanced TNM stage. ESCC patients with high miR-1269 expression had shorter overall survival than those with low miR-1269 expression levels. Compared with the control group, overexpression of miR-1269 promoted cell proliferation, migration, and invasion, while knockdown of miR-1269 inhibited cell proliferation, migration, and invasion. SOX6 was a direct target of miR-1269. Conclusion: These results suggest that miR-1269 plays an important role in the progression of ESCC by targeting SOX6 and may be a potential prognostic biomarker and the miR-1269/SOX6 axis may be a therapeutic target for the patient with ESCC.

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Background Atherosclerosis (AS) is a common frequently-occurring disease in the clinic and a serious threat to human health. This research aimed to explore the value between GASL1 and AS. Methods The expression and values of GASL1 in AS patients were revealed by qRT-PCR and ROC curve. The HUVEC cells were induced by ox-LDL to construct in-vitro models. Cell viability was detected by MTT assay, and apoptosis was detected by flow cytometry. The inflammatory situation was reflected by the ELISA assay. Double luciferase reporter gene assay verified the regulatory relationship between GASL1 and miR-106a, miR-106a and LKB1. Results The levels of GASL1 was lower in AS group than those in control group. The value of GASL1 in predicting AS patients was also tested by the ROC curve. After HUVEC cells were induced by ox-LDL, the levels of GASL1 and LKB1 decreased significantly, while the level of miR-106a increased significantly. Upregulation of LKB1 reversed the effect of upregulation of GASL1 on viability, apoptosis, and inflammation of HUVEC cells induced by ox-LDL. Conclusion Overexpression of GASL1 might suppress ox-LDL-induced HUVEC cell viability, apoptosis, and inflammation by regulating miR-106a/LKB1 axis.