MiR-187-3p Enhances Propranolol Sensitivity of Hemangioma Stem Cells

Infantile hemangioma is the most common soft tissue tumors in childhood. In clinic, propranolol is widely used for infantile hemangioma therapy. However, some of the infantile hemangioma patients display resistance to propranolol treatment. Previous studies show that miR-187-3p is inhibited in hepat...

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Bibliographic Details
Published in:Cell Structure and Function 2019, Vol.44(1), pp.41-50
Main Authors: Liu, Chao, Zhao, Zeliang, Ji, Zhidong, Jiang, Yanyan, Zheng, Jiawei
Format: Article
Language:English
Subjects:
Apoptosis
Base Sequence
Biotin
Caspase
Caspase-3
Cell Proliferation - drug effects
Cell viability
Children
Chromosome 3
Down-Regulation - drug effects
Down-Regulation - genetics
Drug Resistance, Neoplasm - genetics
Hemangioma
Hemangioma - genetics
Hemangioma - pathology
Hepatocellular carcinoma
Humans
Infant
infantile hemangioma
Lung cancer
Lung carcinoma
MicroRNAs - genetics
MiR-187-3p
mRNA
Neoplastic Stem Cells - drug effects
Neoplastic Stem Cells - pathology
NIPBL
Propranolol
Propranolol - pharmacology
Proteins - genetics
resistance
Stem cells
Tumors
Western blotting
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Summary:Infantile hemangioma is the most common soft tissue tumors in childhood. In clinic, propranolol is widely used for infantile hemangioma therapy. However, some of the infantile hemangioma patients display resistance to propranolol treatment. Previous studies show that miR-187-3p is inhibited in hepatocellular carcinoma and lung cancer, while the role of miR-187-3p in infantile hemangioma remains unclear. In the present study, we explore the biological role of miR-187-3p in infantile hemangioma. The mRNA and protein levels of related genes were detected by real-time PCR and Western blotting. CCK8 assay was used to detect cell viability and IC50 values of propranolol. Cell apoptosis was detected by Caspase-3 Activity assay. Luciferase reporter assay and biotin RNA pull down assay were used to detect the interaction between miR-187-3p and the targeted gene. MiR-187-3p was down-regulated in infantile hemangioma tissues and promoted propranolol sensitivity of HemSCs. Mechanically, NIPBL was the direct target of miR-187-3p in HemSCs. NIPBL downregulation inhibited propranolol resistance of HemSCs. Re-introduction of NIPBL reversed miR-187-3p-meidated higher propranolol sensitivity of HemSCs. MiR-187-3p enhanced propranolol sensitivity of hemangioma stem cells via targeting NIPBL. MiR-187-3p may serve as a novel prognostic indicator and potential target for infantile hemangioma therapy.Key words: MiR-187-3p, infantile hemangioma, propranolol, resistance, NIPBL
ISSN:0386-7196
1347-3700
DOI:10.1247/csf.18041