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Characterization of LncRNA SNHG22 as a protector of NKIRAS2 through miR-4492 binding in osteosarcoma.
Zheng, Huo-Liang; Yang, Run-Ze; Xu, Wen-Ning; Liu, Tao; Chen, Peng-Bo; Zheng, Xin-Feng; Li, Bo; Jiang, Lei-Sheng; Jiang, Sheng-Dan.
Afiliación
  • Zheng HL; Department of Clinic of Spine Center, Xinhua Hospital, Shanghai Jiaotong, University School of Medicine, Shanghai 200082, China.
  • Yang RZ; Department of Clinic of Spine Center, Xinhua Hospital, Shanghai Jiaotong, University School of Medicine, Shanghai 200082, China.
  • Xu WN; Department of Clinic of Spine Center, Xinhua Hospital, Shanghai Jiaotong, University School of Medicine, Shanghai 200082, China.
  • Liu T; Department of Clinic of Spine Center, Xinhua Hospital, Shanghai Jiaotong, University School of Medicine, Shanghai 200082, China.
  • Chen PB; Department of Clinic of Spine Center, Xinhua Hospital, Shanghai Jiaotong, University School of Medicine, Shanghai 200082, China.
  • Zheng XF; Department of Clinic of Spine Center, Xinhua Hospital, Shanghai Jiaotong, University School of Medicine, Shanghai 200082, China.
  • Li B; Department of Clinic of Spine Center, Xinhua Hospital, Shanghai Jiaotong, University School of Medicine, Shanghai 200082, China.
  • Jiang LS; Department of Clinic of Spine Center, Xinhua Hospital, Shanghai Jiaotong, University School of Medicine, Shanghai 200082, China.
  • Jiang SD; Department of Clinic of Spine Center, Xinhua Hospital, Shanghai Jiaotong, University School of Medicine, Shanghai 200082, China.
Aging (Albany NY) ; 12(18): 18571-18587, 2020 Sep 20.
Article en En | MEDLINE | ID: mdl-32950969
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.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Prognostic_studies Idioma: En Revista: Aging (Albany NY) Asunto de la revista: GERIATRIA Año: 2020 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
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XML
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Prognostic_studies Idioma: En Revista: Aging (Albany NY) Asunto de la revista: GERIATRIA Año: 2020 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos