lncRNA CASC2 inhibits lipopolysaccharide-induced acute lung injury via miR-27b/TAB2 axis

Long non-coding RNA (lncRNA) cancer susceptibility candidate 2 (CASC2) has been reported to exert an important role in acute lung injury (ALI). The present study aimed to investigate the potential underlying mechanism of CASC2 in ALI progression. Reverse transcription-quantitative PCR was conducted to examine the expression of CASC2, microRNA (miR/miRNA)-27b and TGF-β activated kinase 1 and MAP3K7-binding protein 2 (TAB2) in A549 cells. Cell viability and apoptosis were analyzed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry. Enzyme-linked immunosorbent assay was used to measure the levels of inflammatory-related cytokines to assess the inflammatory response, including interleukin-1β (IL-1β), IL-6 and tumor necrosis factor α (TNF-α). The binding sites of miR-27b in CASC2 or TAB2 were predicted using LncBase or microT-CDS software, following which dual-luciferase reporter and RNA binding protein immunoprecipitation assays were performed to confirm the target relationship between miR-27b and CASC2 or TAB2. The protein expression of TAB2 was detected by western blotting. The decreased viability, and increased apoptosis and inflammatory responses were attenuated by the accumulation of CASC2 in lipopolysaccharide (LPS)-stimulated A549 cells. CASC2 could directly bind to miR-27b in A549 cells. CASC2 protected A549 cells from LPS-triggered injury by downregulating miR-27b. TAB2 was a target of miR-27b in A549 cells. The influence of miR-27b depletion was reversed by the silencing of TAB2 in an ALI cell model. CASC2 could increase the expression of TAB2 by serving as a competing endogenous RNA of miR-27b in A549 cells. Collectively, the results suggested that CASC2 attenuated LPS-induced injury in the ALI cell model by modulating the miR-27b/TAB2 axis.