Trichostatin A‑induced miR‑30a‑5p regulates apoptosis and proliferation of keloid fibroblasts via targeting BCL2.

Keloids are benign fibrous overgrowths that occur as a result of abnormal wound healing following cutaneous injury. MicroRNAs (miRNAs/miRs) are short non‑coding RNAs that serve critical roles in numerous important biological processes, such as cell proliferation, differentiation and apoptosis. However, their role in keloid development remains largely unknown. In the present study, the role of miR‑30a‑5p, a miRNA regulated by Trichostatin A (TSA), in apoptosis within cultured keloid fibroblasts was investigated. An MTT assay was used to detect the proliferation of cultured keloid fibroblasts treated with TSA. Cell apoptosis and cell cycle phases were analyzed using flow cytometry. In addition, an miRNA microarray was performed to compare expression profiles between cultured keloid fibroblasts treated with or without 1,000 nM TSA. Reverse transcription‑quantitative polymerase chain reaction analysis was conducted to estimate miRNA expression levels. The direct target of miR‑30a‑5p was identified using a dual‑luciferase reporter assay. Western blotting was employed to assess protein expression levels in keloid fibroblasts. The results demonstrated that TSA inhibited the proliferation of keloid fibroblasts in a time‑ and dose‑dependent manner. The miRNA microarray revealed alterations in the expression of numerous miRNA sequences in response to TSA when compared with controls. Notably, the expression of miR‑30a‑5p was downregulated in keloid tissues. In addition, overexpression of miR‑30a‑5p induced apoptosis by targeting B‑cell lymphoma 2, which was similar to that observed in response to TSA. These results provide important information regarding a novel miR‑30a‑5p‑mediated signaling pathway induced by TSA treatment, and suggest a potential use for TSA and miR‑30a‑5p as effective therapeutic strategies for keloids.