Acne is a chronic inflammatory skin disease, and the pathogenesis of acne induced by Cutibacterium acnes (C.acnes) is not well understood. Recently, circular RNAs (circRNAs) have attracted much attention because of its involvement in various diseases. However, the mechanisms by which circRNAs regulated acne have rarely been reported. We identified several differentially expressed circRNAs by sequencing patient-derived acne tissues. Among them, hsa_circ_0105040 was determined to be low expressed in acne tissues and localized in the cytoplasm of human primary keratinocytes. We established a C.acnes biofilms model of acne in vitro and showed that hsa_circ_0105040 promoted inflammation via MAPK and NF-κB pathway. Mechanistically, hsa_circ_0105040 could directly bind to miR-146a and inhibit the expression of miR-146a. Moreover, hsa_circ_0105040 promoted the expression of IRAK1 and TRAF6 by sponging miR-146a, thereby elevating the level of inflammation in acne. Collectively, our data suggested that hsa_circ_0105040- miR-146a -IRAK1/TRAF6 axis was involved in regulating the inflammatory response in acne, which provided a potential therapeutic target for acne and a novel insight into the pathogenesis of inflammatory acne.
Keywords: Acne; Inflammation; ceRNA; circRNA; miR-146a.
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