10‑Hydroxycamptothecin induces apoptosis in human fibroblasts by regulating miRNA‑23b‑3p expression

Abstract

10-Hydroxycamptothecin (HCPT) effectively controls epidural fibrosis, but the exact underlying mechanisms remain ambiguous. Abnormal microRNA (miR)‑23b‑3p expression has been detected in various types of fibrotic tissues that are present in different diseases. The aim of the present study was to elucidate the mechanisms through which HCPT induces fibroblast apoptosis. Reverse transcription‑quantitative polymerase chain reactions were performed on six traumatic scar samples and matched normal skin samples; traumatic scar formation was revealed to be significantly inversely associated with miR‑23b‑3p expression. In addition, the miR‑23b‑3p expression level in human fibroblasts was examined following HCPT treatment. The effects of HCPT and miR‑23b‑3p on fibroblast apoptosis were assessed using terminal deoxynucleotidyl‑transferase‑mediated dUTP nick‑end labeling, flow cytometry and western blot analysis. The results demonstrated that HCPT treatment notably increased miR‑23b‑3p expression levels and accelerated fibroblast apoptosis. Therefore, upregulation of miR‑23b‑3p expression was demonstrated to promote fibroblast apoptosis, consistently with the effects of HCPT. The results of the present study indicated that HCPT may induce fibroblast apoptosis by regulating miR‑23b‑3p expression.