Attenuation of sepsis-associated acute lung injury by lncRNA LINC00052 via sponging miR-106b-5p

BACKGROUND: Sepsis-associated acute lung injury (SA-ALI) is a prevalent sequela of sepsis, which imposes a substantial public health burden. Due to the incomplete understanding of its underlying pathogenesis, no fundamental breakthroughs in its treatment have been achieved. To explore the predictive value of LINC00052 and miR-106b-5p in SA-ALI and clarify its mechanism. METHODS: LINC00052 and miR-106b-5p levels were quantified using real-time quantitative polymerase chain reaction (RT-qPCR). The predictive capacity for SA-ALI was assessed using receiver operating characteristic (ROC) curve analysis. Risk factors associated with ALI development were evaluated by Logistic regression. Pearson analysis was conducted to examine the correlation between LINC00052 and clinical indicators. Cellular viability was determined via cell counting kit-8 (CCK-8) assay and flow cytometry, while the concentrations of inflammatory and apoptotic factors were measured using enzyme-linked immunosorbent assay (ELISA) and Western blotting (WB). RESULTS: LINC00052 levels in serum from sepsis patients were lower than in the healthy group and further decreased with the development of SA-ALI, whereas miR-106b-5p expression showed the opposite trend. LINC00052 and miR-106b-5p demonstrated high diagnostic value in distinguishing ALI patients, with enhanced predictive efficacy when combined. LINC00052 expression was inversely correlated with clinical indicators in SA-ALI patients. Mechanistically, upregulation of LINC00052 modulated proliferation, apoptosis, inflammation, and apoptosis markers in A549 cells, an effect cancelled by miR-106b-5p mimic. CONCLUSIONS: LINC00052 functions by sponging miR-106b-5p to suppress apoptosis and mitigate inflammation, with the LINC00052/miR-106b-5p axis exhibits excellent predictive value for SA-ALI, underscoring their clinical relevance as both therapeutic targets and diagnostic biomarkers.