Open AccessCharacterization of LncRNA SNHG22 as a protector of NKIRAS2 through miR-4492 binding in osteosarcoma
Author(s) -
HuoLiang Zheng,
Runze Yang,
Wen-Ning Xu,
Tao Liu,
Pengbo Chen,
Xianxu Zheng,
Bo Li,
LeiSheng Jiang,
ShengDan Jiang
Publication year - 2020
Publication title -
aging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.473
H-Index - 90
ISSN - 1945-4589
DOI - 10.18632/aging.103849
Subject(s) - competing endogenous rna , biology , rna , carcinogenesis , microrna , cancer research , long non coding rna , microbiology and biotechnology , gene , genetics
Many studies have revealed the function of long noncoding RNA (LncRNA) in regulating tumorigenesis of osteosarcoma (OS). As a subgroup of LncRNA, small nucleolar RNA host genes (SNHGs) have emerged as potentially important in OS. According to our recent findings, small nucleolar RNA host gene 22 (SNHG22) plays an important role in inhibiting the growth and metastasis of OS. However, the underlying mechanism of SNHG22 in regulating OS progression remains unknown. In this study, we confirmed that SNHG22 was downregulated in OS, and the overexpression of SNHG22 significantly inhibited OS progression in vivo and in vitro . Meanwhile, overexpression of SNHG22 also inhibited the migration and proliferation of human umbilical vein endothelial cells (HUVECs) and prevented the epithelial-to-mesenchymal transition (EMT) in OS. Furthermore, the interaction between miR-4492 and SNHG22 we previously predicted was validated by RNA pull-down assays and RNA immunoprecipitation assays. Dual-luciferase reporter assays showed that SNHG22 could directly interact with miR-4492 and upregulate the expression of NK-κB inhibitor-interacting Ras-like 2 (NKIRAS2) by its competing endogenous RNA (ceRNA) activity on miR-4492. In conclusion, our study has clarified the function of SNHG22 in OS progression and suggests a novel therapeutic target for OS.