miR‑139‑5p affects cell proliferation, migration and adipogenesis by targeting insulin‑like growth factor 1 receptor in hemangioma stem cells

miR-139-5p 通过靶向血管瘤干细胞中的胰岛素样生长因子 1 受体影响细胞增殖、迁移和脂肪生成

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作者:Yao Wu, Honghong Li, Juan Xie, Fan Wang, Dongsheng Cao, Yin Lou

Abstract

Infant hemangioma is the most common benign tumor in infancy. The pathological development process of this tumor is separated into the proliferation period, the involution period and the composite period in which a few residual capillary‑like vessels grow through the loose fibrofatty tissue. Previous studies have confirmed that insulin‑like growth factor 1 (IGF‑1) is able to facilitate the cell proliferation of hemangioma stem cells (HemSCs) and the differentiation of HemSCs into adipocytes. Additionally, studies have confirmed that microRNAs (miRs) may serve a crucial function in regulating the IGF‑1 receptor (IGF‑1R). miR‑139‑5p often functions as a tumor suppressor. The present study was designed to investigate the mechanism of miR‑139‑5p in HemSCs. Dual luciferase reporter results verified that IGF‑1R is the target gene of miR‑139‑5p. miR‑139‑5p overexpression reduced IGF‑1R expression, and miR‑139‑5p inhibition increased IGF‑1R expression. Cell Counting Kit‑8 and Transwell migration assays demonstrated that miR‑139‑5p overexpression may target IGF‑1R to inhibit the proliferation in addition to the migration of HemSCs. Reverse transcription‑quantitative PCR, oil red o staining and western blot analysis confirmed that miR‑139‑5p overexpression was able to reduce adipogenesis in HemSCs via the IGF‑1/IGF‑1R pathway. In contrary, miR‑139‑5p inhibition substantially enhanced the proliferation, migration and adipogenesis of HemSCs. Overall, miR‑139‑5p is able to affect the IGF‑1/IGF‑1R pathway by regulating IGF‑1R expression, which ultimately affects the proliferation, migration and adipogenesis of HemSCs.

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