The abnormal upregulation of transforming growth factor-β (TGF-β) signaling has been demonstrated to initiate keloid formation and progression. Keloid is a type of benign skin tumor that may occur following sustaining skin injury. microRNA-96 (miR-96) serves an important role in the progression of various malignant diseases. Using reverse transcription quantitative polymerase chain reaction (RT-qPCR), the present study demonstrated that miR-96 was overexpressed in keloid-derived fibroblasts (KFs). Luciferase reporter assay revealed mothers against decapentaplegic homolog (Smad)7, which is one of the important inhibitory factors in the TGF-β pathway, as a direct target of miR-96. miR-96 was initially observed to be correlated with the deposition of type I collagen in KFs in vitro. The miR-96 antagomir, was directly added into the keloid organ culture (OC) to find its significant antifibrotic potential, such as keloid OC shrinkage, exhibited by its dry weight loss and improved dermis architecture, exhibited by Masson's staining. Following miR-96 antagomir treatment, a reduction in the mRNA and protein expression levels of collagen type I α 1 chain and collagen type 3 α 1 chain within keloid OC tissues was observed. The present study revealed that miR-96 serves an important role in pathogenic keloid formation, suggesting that miR-96 antagomir has the potential to prevent keloid progression.
Keywords: benign tumor; keloid; microRNA-96; mothers against decapentaplegic homolog 7; skin fibroblasts.