MicroRNA-98 suppresses cell growth and invasion of retinoblastoma via targeting the IGF1R/k-Ras/Raf/MEK/ERK signaling pathway
| Autor: | Hong Ma, Yu Bai, Shuzhe Ji, Long Guo |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Male Cancer Research Cell Survival Cell Apoptosis Mitogen-activated protein kinase kinase Biology retinoblastoma Receptor IGF Type 1 03 medical and health sciences 0302 clinical medicine Cell Movement Cell Line Tumor medicine Humans insulin-like growth factor-1 receptor/k-Ras/Raf/mitogen activated protein kinase kinase/extracellular signal-regulated kinase signaling pathway Neoplasm Invasiveness Viability assay prognostic biomarker Child Insulin-like growth factor 1 receptor microRNA-98 Cell Proliferation Oncogene Cell growth Infant Newborn Infant Receptors Somatomedin Articles Cell cycle Gene Expression Regulation Neoplastic Survival Rate MicroRNAs 030104 developmental biology medicine.anatomical_structure Oncology 030220 oncology & carcinogenesis Child Preschool Cancer research Female Signal transduction Protein Binding Signal Transduction |
| Zdroj: | International Journal of Oncology |
| ISSN: | 1791-2423 1019-6439 |
| Popis: | Accumulating evidence has indicated that the dysregulation of microRNAs (miRNAs) is involved in the pathogenesis o retinoblastoma (RB); however, the potential role of miR‑98 in RB remains elusive. In the present study, it was demonstrated that miR‑98 is downregulated in RB tissues and cell lines, and its expression significantly associated with clinicopathological features, including differentiation, N classification and largest tumor base; patients with low miR‑98 expression levels exhibited significantly poorer overall survival. Overexpression of miR‑98 was suggested to suppress RB cell growth, migration and invasion. In addition, insulin‑like growth factor‑1 receptor (IGF1R), a well‑reported oncogene, was identified as a potential target of miR‑98 via a luciferase assay, reverse transcription‑quantitative polymerase chain reaction and western blotting. Correlation analysis revealed a significantly negative correlation between miR‑98 and IGF1R expression in tumor tissues (n=60). In addition, the results of the present study demonstrated that IGF1R function as an oncogene by promoting RB cell viability, migration and invasion. Furthermore, restoration of IGF1R was observed to reverse the anticancer effects of miR‑98 on RB cell viability, migration and invasion. Importantly, the findings of the present study indicated that miR‑98 suppressed RB cell growth and metastasis by inhibiting the IGF1R/k‑Ras/Raf/mitogen activated protein kinase kinase/extracellular signal‑regulated kinase signaling pathway. Collectively, the present study proposed that miR‑98 may serve as a novel prognostic biomarker and therapeutic target in the treatment of RB. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|