Long non-coding RNA CASC7 Contributes to the Progression of Sepsis-Induced Liver Injury by Targeting miR-217/TLR4 Axis

Abstract Background: Sepsis is a system inflammation disease that can lead to liver injury. Long non-coding RNAs as crucial regulators participate in the regulation of sepsis-induced liver injury. However, the role of lncRNA CASC7 (CASC7) in the modulation of sepsis-induced liver injury remains elusive. Here, we aimed to explore the effect of CASC7 on the sepsis-induced liver injury. Methods: The sepsis mouse model was established in BALB/c mice by the treatment of lipopolysaccharide (LPS). The effect of CASC7 on sepsis-induced liver injury was analyzed by Hematoxylin and Eosin (HE) staining, ELISA assays, TUNEL detection kit, CCK‐8 assays, and Annexin V-FITC Apoptosis Detection Kit in vivo or in vitro . The mechanism investigation was performed using RNA pull-down, luciferase reporter gene assays, qPCR assays, and Western blot analysis. Results: The expression of CASC7 was elevated in a time-dependent manner in the liver tissues of the sepsis mice and LPS-treated LO2 cells. The depletion of CASC7 decreased the LPS treatment-induced liver injury in the sepsis mice. The treatment of LPS enhanced the apoptosis in the sepsis mice, while the depletion of CASC7 blocked this enhancement in the system. The CASC7 knockdown inhibited the LPS-enhanced expression of TNF-α and IL-1β in the mice. CASC7 served as a sponge for the miR-217 in the liver cells. CASC7 promoted the progression of sepsis-induced liver injury by sponging miR-217. MiR-217 attenuated sepsis-induced liver injury by targeting TLR4. Conclusions: Thus, we conclude that CASC7 contributes to the progression of sepsis-induced liver injury by targeting miR-217/TLR4 axis.