miR‑497/MIR497HG inhibits glioma cell proliferation by targeting CCNE1 and the miR‑588/TUSC1 axis

Oncol Rep. 2021 Dec;46(6):255. doi: 10.3892/or.2021.8206. Epub 2021 Oct 19.

Abstract

Emerging evidence has shown that microRNA (miR)‑497 serves pivotal roles in tumorigenesis, cancer progression, metastasis and chemotherapy resistance in several types of cancer. In the present study, the expression and biological functions of miR‑497 host gene (MIR497HG) were investigated in glioma tissue. The expression levels of miR‑497 and MIR497HG were measured in glioma, adjacent non‑cancerous and normal brain tissue and their association with the prognosis of patients with glioma were analyzed. The biological roles of miR‑497 and MIR497HG were investigated in glioma cell lines. In addition, bioinformatics analysis, luciferase reporter assay and functional experiments were performed to identify and validate the downstream targets of miR‑497 or MIR497HG. The expression levels of miR‑497 and MIR497HG were downregulated in glioma tissue and cell lines compared with those in adjacent non‑cancerous and normal brain tissue and normal human cortical neuron cell line. Patients with low miR‑497 or MIR497HG expression levels exhibited a poor prognostic outcome. In addition, forced overexpression of miR‑497 or MIR497HG significantly inhibited the proliferation and cell cycle progression of glioma cell lines. Furthermore, the results indicated that miR‑497 and MIR497HG exerted their biological functions by direct targeting of cyclin E1 and miR‑588/tumor suppressor candidate 1. In summary, the data indicated that miR‑497 and MIR497HG served as tumor suppressors and may be used as potential therapeutic targets and prognostic biomarkers in glioma.

Keywords: MIR497HG; cyclin E1; glioma; miR‑497; miR‑588; tumor suppressor candidate 1.

MeSH terms

  • Adult
  • Animals
  • Brain Neoplasms / genetics
  • Carcinogenesis / genetics
  • Cell Cycle / genetics
  • Cell Line, Tumor
  • Cell Proliferation / genetics*
  • Cyclin E / genetics*
  • Disease Models, Animal
  • Down-Regulation
  • Female
  • Gene Expression Regulation, Neoplastic
  • Glioma / genetics*
  • Humans
  • Male
  • Mice
  • Mice, Nude
  • MicroRNAs / genetics*
  • Middle Aged
  • Oncogene Proteins / genetics*
  • Tumor Suppressor Proteins / genetics*

Substances

  • CCNE1 protein, human
  • Cyclin E
  • MIRN497 microRNA, human
  • MIRN588 microRNA, human
  • MicroRNAs
  • Oncogene Proteins
  • TUSC1 protein, human
  • Tumor Suppressor Proteins

Grants and funding

The present study was supported by grants from National Natural Science Foundation of China (grant no. 81502145) and National Natural Science Foundation of Shaanxi (grant no. 2016JQ8017).