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

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.