LOC102553417 silencing facilitates the apoptosis of hepatic stellate cells via the miR‑30e/MTDH axis.

Abstract

Hepatic fibrosis is an inevitable pathological process in the progression of multiple chronic liver diseases and remains a major challenge in the treatment of liver diseases. The purpose of the present study was to demonstrate whether silencing of the long non-coding RNA LOC102553417 promoted hepatic stellate cell (HSC) apoptosis via the microRNA (miR)-30e/metadherin (MTDH) axis. A LOC102553417 silencing lentivirus was constructed and transduced into HSC-T6 cells. After confirming the silencing efficiency by reverse transcription-quantitative PCR, cell proliferation was assessed using the Cell Counting Kit-8 assay and apoptosis was assessed using flow cytometry. The interaction between LOC102553417 and miR-30e, and that between miR-30e and MTDH, was demonstrated using the dual-luciferase reporter assay and RNA binding protein immunoprecipitation. The apoptosis of HSC-T6 cells was detected after transfection of miR-30e mimics and inhibitors with or without silencing LOC102553417. Silencing of LOC102553417 curbed HSC-T6 cell proliferation and expedited their apoptosis. LOC102553417 was demonstrated to target miR-30e, whereas miR-30e targeted MTDH. In addition, LOC102553417 silencing significantly upregulated miR-30e expression levels, and significantly downregulated MTDH mRNA and protein expression levels, which resulted in a significantly reduced p-Akt/Akt ratio and significantly elevated p53 protein expression levels. Transfection with miR-30e mimic alone significantly enhanced HSC-T6 cell apoptosis and inhibits LOC102553417 and MTDH expressions, In addition, miR-30e mimic expedites the apoptosis of HSCs stimulated by LOC102553417 silencing; consistent results were obtained by reverse validation of miR-30e inhibitor. In conclusion, the present study demonstrated that LOC102553417 silencing stimulated the apoptosis of HSCs via the miR-30e/MTDH axis.