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Keloids are very resistant to treatment in dermatology and plastic surgical practice. The present study aimed to explore the underlying mechanism of botulinum toxin A (BTXA) treated human skin keloid fibroblasts (HSFBs) proving some new insights into keloids treatment. Expression of miR-1587 and miR-2392 were significantly down-regulated in keloid tissues and HSFBs, while the ZEB2 was a target of both and up-regulated in keloid tissues and HSFBs compared with the normal controls. BTXA could significantly increase the expression of miR-1587 and miR-2392 but decrease the expression of ZEB2. BTXA could significantly inhibit the proliferation, cell cycle, and migration and promote apoptosis and autophagy of HSFBs; however, miR-1587 and miR-2392 inhibitors could reverse these effects of BTXA on HSFBs. Silencing ZEB2 could significantly attenuate the effects of miR-1587 and miR-2392 inhibitors in promoting cell proliferation and migration and suppressing apoptosis and autophagy of HSFBs after treating with BTXA. BTXA could suppress the proliferation and migration and promote apoptosis and autophagy of HSFBs via modulating miR-1587/miR-2392 targeted ZEB2.

BTXA regulates the epithelial–mesenchymal transition and autophagy of keloid fibroblasts via modulating miR-1587/miR-2392 targeted ZEB2