MicroRNA-598 acts as an inhibitor in retinoblastoma through targeting E2F1 and regulating AKT pathway
| Autor: | Yan Liang, Qi Zhang, Fengge Liu |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Retinal Neoplasms Apoptosis Biochemistry 03 medical and health sciences 0302 clinical medicine Cell Movement microRNA medicine Biomarkers Tumor Tumor Cells Cultured E2F1 Humans Viability assay E2F Molecular Biology Protein kinase B Transcription factor PI3K/AKT/mTOR pathway Cell Proliferation Retinoblastoma Chemistry Cell Biology medicine.disease Prognosis Gene Expression Regulation Neoplastic MicroRNAs 030104 developmental biology 030220 oncology & carcinogenesis Cancer research Proto-Oncogene Proteins c-akt E2F1 Transcription Factor |
| Zdroj: | Journal of cellular biochemistryREFERENCES. 121(3) |
| ISSN: | 1097-4644 |
| Popis: | Recently, microRNAs (miRNAs) receive more attention due to their role in the pathogenesis of malignancies. Retinoblastoma (RB) is the most serious and harmful malignant tumor in infants and young children with eye diseases, which often endangers the lives of children. This study was designed to determine how miR-598 is involved in RB progression. In this study, quantitative reverse transcription-polymerase chain reaction, Western blot, dual-luciferase reporter, Cell Counting Kit-8, and Transwell assays were adopted to detect miR-598 expression and function in RB. The decreased expression of miR-598 was identified in RB. Overexpression of miR-598 suppressed the viability and metastasis of RB cells. Further, E2F transcription factor 1 (E2F1) is verified as a direct target of miR-598. Furthermore, E2F1 recovered miR-598-mediated-inhibition of cell viability and metastasis in RB. In addition, miR-598 was found to promote cell apoptosis and inactivate the protein kinase B (AKT) pathway in RB. miR-598 suppressed RB cell viability and metastasis through inhibiting E2F1 and inactivating AKT pathway, which may provide a new perspective for RB treatment. |
| Databáze: | OpenAIRE |
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