BMB Reports 2019; 52(3): 202-207
MicroRNA-152-5p inhibits proliferation and migration and promotes apoptosis by regulating expression of Smad3 in human keloid fibroblasts
Qianqian Pang1, Yuming Wang1, Mingyuan Xu1, Jiachao Xu2, Shengquan Xu3, Yichen Shen1, Jinghong Xu1,* & Rui Lei1
1Department of Plastic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, 2Department of Internal Medicine, Haiyan Hospital of Traditional Chinese Medicine, Jiaxin 314300, 3Department of Hand Surgery and Microsurgery Center, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China
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Received: December 4, 2018; Revised: December 28, 2018; Accepted: January 5, 2019; Published online: March 31, 2019.
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Keloids are the most common pathological form of trauma healing, with features that seriously affect appearance and body function, are difficult to treat and have a high recurrence rate. Emerging evidence suggests that miRNAs are involved in a variety of pathological processes and play an important role in the process of fibrosis. In this study, we investigated the function and regulatory network of miR-152-5p in keloids. The miRNA miR-152-5p is frequently downregulated in keloid tissue and primary cells compared to normal skin tissue and fibroblasts. In addition, the downregulation of miR-152-5p is significantly associated with the proliferation, migration and apoptosis of keloid cells. Overexpression of miR-152-5p significantly inhibits the progression of fibrosis in keloids. Smad3 is a direct target of miR-152-5p, and knockdown of Smad3 also inhibits fibrosis progression, consistent with the overexpression of miR-152-5p. The interaction between miR-152-5p and Smad3 occurs through the Erk1/2 and Akt pathways and regulates collagen3 production. In summary, our study demonstrates that miR-152-5p/Smad3 regulatory pathways involved in fibrotic progression may be a potential therapeutic target of keloids.
Keywords: Apoptosis, Keloid, miR-152-5p, Proliferation, Smad3

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