Adenosine Deaminase Acting on RNA1 (ADAR1) Deficiency Promotes Proliferation of Hemangioma-Derived Endothelial Cells via PI3K/Akt/mTOR Pathway
Adenosine Deaminase Acting on RNA1 (ADAR1) Deficiency Promotes Proliferation of Hemangioma-Derived Endothelial Cells via PI3K/Akt/mTOR Pathway
Chaoqi Yin1*, Ruyi Tao1, Kaixi Tan2 and Jianfei Zhang3
ABSTRACT
Infantile hemangioma (IH) is one of the most common benign tumours occurs in infancy. The adenosine deaminase acting on RNA1 (ADAR1) activates phosphorylated Akt (p-Akt), but the roles of ADAR1 remain unknown in IH. The objective of this study was to investigate the expression level and functions of ADAR1. Immunohistochemical method and western blotting were used to detect the protein levels of ADAR1 in human IH tissues. ADAR1-targeted siRNAs were transfected into HemECs cells to knockdown the expression of ADAR1. CCK-8 assay and cell tubule formation assay were performed to detect the phenotypic change after knockdown of ADAR1 expression. Western blotting was used to detect the related factors of Akt/mTOR signalling pathway. The expression level of ADAR1 is significantly up-regulated in the IH tissues as compared to the adjacent tissues. A sharp decrease of proliferation and cell tubule formation abilities was observed after knockdown of ADAR1 using ADAR1-targeted siRNAs. The expression levels of p-Akt, Akt, and mTOR were significantly inhibited after knockdown of ADAR1. It was concluded that ADAR1 is highly expressed in IH. Knockdown of ADAR1 inhibits cell proliferation and cell tubule formation abilities through down-regulation of Akt/mTOR signalling pathway.
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