lncRNA SNHG16 promotes glioma tumorigenicity through miR-373/EGFR axis by activating PI3K/AKT pathway
| Autor: | Xiang-Yang Zhou, Hong Liu, Hai-Peng Xi, Guang-Wei Wang, Zheng-Bin Ding |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0106 biological sciences
Brain tumor Host gene Biology medicine.disease_cause 01 natural sciences Cell Line 03 medical and health sciences Phosphatidylinositol 3-Kinases Cell Movement Glioma Genetics medicine Humans Neoplasm Invasiveness Small nucleolar RNA PI3K/AKT/mTOR pathway Cells Cultured 030304 developmental biology Cell Proliferation 0303 health sciences Competing endogenous RNA Brain Neoplasms medicine.disease ErbB Receptors Gene Expression Regulation Neoplastic MicroRNAs Cancer research RNA Long Noncoding Carcinogenesis Proto-Oncogene Proteins c-akt Function (biology) 010606 plant biology & botany Signal Transduction |
| Zdroj: | Genomics. 112(1) |
| ISSN: | 1089-8646 |
| Popis: | Glioma is one of the most common and aggressive malignant primary brain tumor with invariably poor 5-year survival rates. Because of the high recurrence rate and mortality rate, effective therapies for glioma are still weak. Recently, several studies has been proved that long non-coding RNAs (lncRNAs) have been identified to play regulatory mediators in the tumorigenesis of glioma. Nevertheless, the role of lncRNAs and their downstream transcripts are still elusive in the progression of glioma. Small nucleolar RNA host gene 16 (SNHG16), a newly identified lncRNA, has been verified to be up-regulated in human malignant carcinomas. In the present study, we confirmed that lncRNA SNHG16 was highly expressed in glioma and may exert oncogenic function as a competing endogenous RNA (ceRNA) to regulate EGFR by sponging of miR-373-3p through activating PI3K/AKT pathway, which providing a new insight of the regulatory network of lncRNA SNHG16 in the development of glioma. |
| Databáze: | OpenAIRE |
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