MicroRNA‑98 suppresses cell growth and invasion of retinoblastoma via targeting the IGF1R/k‑Ras/Raf/MEK/ERK signaling pathway

Long Guo, Yu Bai, Shuzhe Ji, Hong Ma

Research output: Contribution to journalArticlepeer-review

11 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)807-820
Number of pages14
JournalInternational journal of oncology
Volume54
Issue number3
DOIs
StatePublished - Mar 2019

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

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