{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,13]],"date-time":"2026-06-13T21:48:32Z","timestamp":1781387312381,"version":"3.54.1"},"reference-count":39,"publisher":"Baishideng Publishing Group Inc.","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["World J Stem Cells"],"abstract":"BACKGROUND<\/jats:p>\n Acute lung injury (ALI) is a fatal and heterogeneous disease. While bone marrow mesenchymal stem cells (BMSCs) have shown promise in ALI repair, their efficacy is compromised by a high apoptotic percentage. Preliminary findings have indicated that long noncoding RNA (lncRNA)-ENST expression is markedly downregulated in MSCs under ischemic and hypoxic conditions, establishing a rationale for in vitro exploration.<\/jats:p>\n AIM<\/jats:p>\n To elucidate the role of lncRNA-ENST00000517482 (lncRNA-ENST) in modulating MSC apoptosis.<\/jats:p>\n METHODS<\/jats:p>\n Founded on ALI in BEAS-2B cells with lipopolysaccharide, this study employed a transwell co-culture system to study BMSC tropism. BMSCs were genetically modified to overexpress or knockdown lncRNA-ENST. After analyzing the effects on autophagy, apoptosis and cell viability, the lncRNA-ENST\/miR-539\/c-MYC interaction was confirmed by dual-luciferase assays.<\/jats:p>\n RESULTS<\/jats:p>\n These findings have revealed a strong correlation between lncRNA-ENST levels and the apoptotic and autophagic status of BMSCs. On the one hand, the over-expression of lncRNA-ENST, as determined by Cell Counting Kit-8 assays, increased the expression of autophagy markers LC3B, ATG7, and ATG5. On the other hand, it reduced apoptosis and boosted BMSC viability. In co-cultures with BEAS-2B cells, lncRNA-ENST overexpression also improved cell vitality. Additionally, by downregulating miR-539 and upregulating c-MYC, lncRNA-ENST was found to influence mitochondrial membrane potential, enhance BMSC autophagy, mitigate apoptosis and lower the secretion of pro-inflammatory cytokines interleukin-6 and interleukin-1\u03b2. Collectively, within the in vitro framework, these results have highlighted the therapeutic potential of BMSCs in ALI and the pivotal regulatory role of lncRNA-ENST in miR-539 and apoptosis in lipopolysaccharide-stimulated BEAS-2B cells.<\/jats:p>\n CONCLUSION<\/jats:p>\n Our in vitro results show that enhanced lncRNA ENST expression can promote BMSC proliferation and viability by modulating the miR-539\/c-MYC axis, reduce apoptosis and induce autophagy, which has suggested its therapeutic potential in the treatment of ALI.<\/jats:p>","DOI":"10.4252\/wjsc.v17.i3.100079","type":"journal-article","created":{"date-parts":[[2025,3,19]],"date-time":"2025-03-19T09:40:27Z","timestamp":1742377227000},"source":"Crossref","is-referenced-by-count":2,"title":["Regulation of lncRNA-ENST on Myc-mediated mitochondrial apoptosis in mesenchymal stem cells: In vitro<\/i> evidence implicated for acute lung injury therapeutic 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