Open AccessmiR‑139‑5p affects cell proliferation, migration and adipogenesis by targeting insulin‑like growth factor 1 receptor in hemangioma stem cells
Author(s) -
Yao Wu,
Honghong Li,
Juan Xie,
Fan Wang,
Dongsheng Cao,
Yin Lou
Publication year - 2019
Publication title -
international journal of molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.048
H-Index - 90
eISSN - 1791-244X
pISSN - 1107-3756
DOI - 10.3892/ijmm.2019.4430
Subject(s) - adipogenesis , cell cycle , cell growth , biology , growth factor , cancer research , microrna , oncogene , microbiology and biotechnology , cell migration , insulin like growth factor , stem cell , cell , receptor , mesenchymal stem cell , gene , biochemistry , genetics
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.