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USP18 promotes the growth in hemangiomas by regulating PI3K/AKT pathway
Ke Huan,Ma Xiang,Zeng Ying,Lu Jingjing,Fu Guili 대한독성 유전단백체 학회 2021 Molecular & cellular toxicology Vol.17 No.4
Background USP (ubiquitin-specific peptidase) 18 functions as deubiquitinating enzyme and participates in various human malignancies. The underlying mechanism involved in USP18-mediated hemangiomas progression has not been reported yet. Objective Immunohistochemistry analysis, qRT-PCR, and western blot were applied to detect USP18 expression in hemangioma tissues and cells. Lentiviral-mediated short hairpin RNA transfection was performed to silence USP18, and pcDNA-mediated USP18 over-expression was also performed. Cell Counting Kit-8 (CCK-8), colony formation assay and flow cytometry were applied to investigate cell viability, proliferation, and apoptosis, respectively. In vivo xenograft model was performed to detect function of USP18 on tumor growth. Results USP18 was enhanced in hemangioma tissues and cells compared to vascular endothelial tissues and vascular endothelial cells, respectively. Forced USP18 promoted cell viability and proliferation of human hemangioma endothelial cell (HemEC) and hemangioendothelioma endothelial cell (EOMA). Cell apoptosis of HemEC and EOMA were repressed by USP18 over-expression with reduced Bax and cleaved caspase-3. In contrast, silence of USP18 demonstrated the opposite effects on HemEC and EOMA cell viability, proliferation, and apoptosis. Silence of USP18 also retarded in vivo tumorigenicity of hemangiomas. Phosphorylation of AKT was enhanced by USP18 over-expression, while reduced by USP18 silence. Conclusion USP18 functioned as an oncogene in hemangiomas through acceleration of cell proliferation and repression of cell apoptosis, providing new insight for therapy of hemangiomas. Background USP (ubiquitin-specific peptidase) 18 functions as deubiquitinating enzyme and participates in various human malignancies. The underlying mechanism involved in USP18-mediated hemangiomas progression has not been reported yet. Objective Immunohistochemistry analysis, qRT-PCR, and western blot were applied to detect USP18 expression in hemangioma tissues and cells. Lentiviral-mediated short hairpin RNA transfection was performed to silence USP18, and pcDNA-mediated USP18 over-expression was also performed. Cell Counting Kit-8 (CCK-8), colony formation assay and flow cytometry were applied to investigate cell viability, proliferation, and apoptosis, respectively. In vivo xenograft model was performed to detect function of USP18 on tumor growth. Results USP18 was enhanced in hemangioma tissues and cells compared to vascular endothelial tissues and vascular endothelial cells, respectively. Forced USP18 promoted cell viability and proliferation of human hemangioma endothelial cell (HemEC) and hemangioendothelioma endothelial cell (EOMA). Cell apoptosis of HemEC and EOMA were repressed by USP18 over-expression with reduced Bax and cleaved caspase-3. In contrast, silence of USP18 demonstrated the opposite effects on HemEC and EOMA cell viability, proliferation, and apoptosis. Silence of USP18 also retarded in vivo tumorigenicity of hemangiomas. Phosphorylation of AKT was enhanced by USP18 over-expression, while reduced by USP18 silence. Conclusion USP18 functioned as an oncogene in hemangiomas through acceleration of cell proliferation and repression of cell apoptosis, providing new insight for therapy of hemangiomas.
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