Abstract Objectives To investigate the diagnostic value of long non-coding RNA MSC antisense RNA 1 (MSC-AS1) for type 2 diabetes mellitus (T2DM) and its regulatory effect on pancreatic β-cell function. Methods A total of 132 patients with T2DM were enrolled, and 5 mL of fasting venous blood was collected. Receiver operating characteristic (ROC) curves were used to assess the diagnostic value of MSC-AS1 for T2DM, while logistic regression identified risk factors. An in vitro high-glucose model was established in MIN6 cells treated with 25 mM glucose. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to measure the expression of target genes, cell counting kit-8 (CCK-8) assessed cell proliferation, and enzyme-linked immunosorbent assay (ELISA) evaluated insulin and inflammatory cytokine secretion. Dual luciferase reporter assay and RNA immunoprecipitation assay validated gene interactions. Results MSC-AS1 was downregulated in the serum of T2DM patients and high glucose (HG)-induced MIN6 cells. It negatively correlated with glycemic indicators, including fasting blood glucose (FBG) and glycated hemoglobin (HbA1C). ROC analysis demonstrated MSC-AS1’s diagnostic value for predicting T2DM. We identified MSC-AS1 as a protective factor against T2DM onset. Transfection with oe-MSC-AS1 promoted HG-induced MIN6 cell proliferation and insulin secretion while reducing inflammation levels. As a target gene of MSC-AS1, miR-103a-3p could counteract the protective effects of MSC-AS1 overexpression on MIN6 cells. Conclusions MSC-AS1 may facilitate MIN6 proliferation and insulin secretion and could attenuate inflammation via miR-103a-3p, which might be implicated in delaying T2DM progression.
Su et al. (Tue,) studied this question.
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