• Analytical biochemistry · Aug 2021

    LINC01116 regulates proliferation, migration, and apoptosis of keloid fibroblasts by the TGF-β1/SMAD3 signaling via targeting miR-3141.

    • Dan Wu, JinJie Zhou, Ming Tan, and Yanshijing Zhou.
    • Department of Plastic and Cosmetic Surgery, Maternal and Child Health Hospital of Hubei Province, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430070, China.
    • Anal. Biochem. 2021 Aug 15; 627: 114249.

    BackgroundKeloids are benign fibroproliferative skin tumors. Long non-coding RNAs (lncRNAs) have been implicated in the pathogenesis of keloid formation. In this paper, we explored the precise actions of LINC01116 in keloid formation.MethodsThe targeted relationship between microRNA (miR)-3141 and LINC01116 or transforming growth factor β1 (TGF-β1) was verified by dual-luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays. The expression levels of LINC01116, miR-3141, TGF-β1, and SMAD family member 3 (SMAD3) were gauged by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. Cell proliferation, migration, and apoptosis were assessed by the Cell Counting Kit-8 (CCK-8) assay, wound-healing assay, and flow cytometry, respectively. Animal studies were used to assess the role of LINC01116 in the subcutaneous keloid growth in vivo.ResultsOur data showed that LINC01116 targeted miR-3141 by directly binding to miR-3141. LINC01116 was up-regulated and miR-3141 was down-regulated in human keloid tissues and fibroblasts. LINC01116 knockdown or miR-3141 overexpression suppressed keloid fibroblast proliferation, migration, and promoted cell apoptosis. Moreover, miR-3141 was a downstream mediator of LINC01116 function. MiR-3141 regulated the TGF-β1/SMAD3 signaling by directly targeting TGF-β1. Furthermore, TGF-β1 was identified as a direct and functional target of miR-3141. LINC01116 regulated the TGF-β1/SMAD3 signaling through miR-3141. Additionally, LINC01116 knockdown diminished the subcutaneous keloid growth in vivo.ConclusionOur findings demonstrated a novel mechanism, the miR-3141/TGF-β1/SMAD3 regulatory pathway, at least partially for the oncogenic role of LINC01116 in keloid formation.Copyright © 2021 Elsevier Inc. All rights reserved.

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