SNHG16 Silencing Inhibits Neuroblastoma Progression by Downregulating HOXA7 via Sponging miR-128-3p
| Autor: | Qinglei Meng, Shufeng Zhang, Tao Qin, Juntao Bao |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Down-Regulation Apoptosis Biochemistry Flow cytometry Neuroblastoma 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine Cell Movement Cell Line Tumor Human Umbilical Vein Endothelial Cells medicine Animals Humans Gene silencing Cell Proliferation Homeodomain Proteins Mice Inbred BALB C Gene knockdown Messenger RNA Reporter gene medicine.diagnostic_test Cell growth Chemistry General Medicine medicine.disease Molecular biology Gene Expression Regulation Neoplastic MicroRNAs 030104 developmental biology RNA Long Noncoding 030217 neurology & neurosurgery |
| Zdroj: | Neurochemical Research. 45:825-836 |
| ISSN: | 1573-6903 0364-3190 |
| DOI: | 10.1007/s11064-020-02955-x |
| Popis: | Neuroblastoma (NB) is a common intracranial solid tumor with high mortality. Small nucleolar RNA host gene 16 (SNHG16), one of the long noncoding RNAs (lncRNAs), has been reported to be linked to the poor prognosis of NB. However, the mechanisms of SNHG16 in regulating NB progression remain poorly understood. The expression level of SNHG16 was measured by quantitative real time polymerase chain reaction (qRT-PCR). The starBase was employed to predict the interaction of miR-128-3p and SNHG16 or HOXA7, which was verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Cell proliferation and apoptosis were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry, respectively. Transwell assay was used to detect cell invasion or migration. The mRNA and protein levels of homeobox protein A7 (HOXA7) were determined by qRT-PCR and western blot, respectively. The levels of SNHG16 and HOXA7 were conspicuously increased in NB tissues and cells, while the expression of miR-128-3p was obviously declined, compared with corresponding normal tissues and cells. SNHG16 silencing inhibited proliferation, migration and invasion and induced apoptosis of NB cells. We identified that SNHG16 directly interacted with miR-128-3p, and miR-128-3p could target the 3'UTR of HOXA7 in NB cells. Simultaneously, miR-128-3p expression was negatively associated with SNHG16 or HOXA7. Further studies indicated that SNHG16 overexpression rescued the effects of miR-128-3p-mediated on inhibiting proliferation, migration, invasion and promoting apoptosis of NB cells. Moreover, SNHG16 could modulate HOXA7 by sponging miR-128-3p in NB cells. Besides, SNHG16 silencing suppressed tumor growth in vivo. Knockdown of SNHG16 impeded proliferation, migration, invasion and induced apoptosis through the SNHG16/miR-128-3p/HOXA7 axis in NB cells. |
| Databáze: | OpenAIRE |
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