SNHG16 knockdown inhibits tumorigenicity of neuroblastoma in children via miR-15b-5p/PRPS1 axis
| Autor: | Jing Bi, Mei Rao, Yuli Yu, Sihai Tan, Yirong Ge, Lidan Tian |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Male
0301 basic medicine Carcinogenesis Cell Flow cytometry Mice Neuroblastoma 03 medical and health sciences 0302 clinical medicine Downregulation and upregulation Cell Line Tumor Human Umbilical Vein Endothelial Cells Ribose-Phosphate Pyrophosphokinase medicine Animals Humans Child Mice Inbred BALB C Gene knockdown Reporter gene medicine.diagnostic_test Brain Neoplasms Cell growth Chemistry General Neuroscience Cell cycle medicine.disease Xenograft Model Antitumor Assays MicroRNAs 030104 developmental biology medicine.anatomical_structure Gene Knockdown Techniques Cancer research RNA Long Noncoding 030217 neurology & neurosurgery |
| Zdroj: | NeuroReport. 31:1225-1235 |
| ISSN: | 0959-4965 |
| DOI: | 10.1097/wnr.0000000000001537 |
| Popis: | Neuroblastoma is an important problem in children. Long noncoding RNAs (lncRNAs) exhibit important roles in tumorigenicity of neuroblastoma. However, the role and mechanism of lncRNA small nucleolar RNA host gene 16 (SNHG16) in neuroblastoma tumorigenicity remain poorly understood. Forty-six neuroblastoma samples and 28 normal tissues were harvested. The levels of SNHG16, microRNA-15b-5p (miR-15b-5p), and phosphoribosyl pyrophosphate synthetase 1 (PRPS1) were detected via quantitative reverse transcription PCR or western blot. Cell proliferation as well as cycle distribution were measured via 3-(4, 5-Dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide or flow cytometry. Cell metastasis was investigated via epithelial-mesenchymal transition or transwell assay. The target relationship of miR-15b-5p and SNHG16 or PRPS1 was explored via starBase and dual-luciferase reporter assay. The role of SNHG16 in neuroblastoma in vivo was analyzed using a xenograft model. We found SNHG16 and PRPS1 levels were increased in neuroblastoma tissues and cells. SNHG16 knockdown inhibited cell proliferation, increased the cell cycle distribution at G0/G1 phase, and decreased the cells at S phase. SNHG16 overexpression caused an opposite effect. SNHG16 silence suppressed neuroblastoma cell metastasis. PRPS1 knockdown constrained cell proliferation and metastasis and regulated cell cycle distribution. miR-15b-5p was sponged by SNHG16 and directly targeted PRPS1. miR-15b-5p knockdown or PRPS1 overexpression mitigated the influence of SNHG16 silence on cell cycle, proliferation, and metastasis. SNHG16 knockdown reduced xenograft tumor growth. In conclusion, SNHG16 downregulation suppressed neuroblastoma tumorigenicity by regulating cell cycle, proliferation, and metastasis via miR-15b-5p/PRPS1 axis. |
| Databáze: | OpenAIRE |
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