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Updated: Dec 31, 2025

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
miR‑139‑5p affects cell proliferation, migration and adipogenesis by targeting insulin‑like growth factor 1 receptor
Yao Wu1, Honghong Li1, Juan Xie1
1Department of Plastic Surgery, The Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, P.R. China.
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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