MicroRNA-192 promotes the development of nasopharyngeal carcinoma through targeting RB1 and activating PI3K/AKT pathway

World J Surg Oncol. 2020 Feb 3;18(1):29. doi: 10.1186/s12957-020-1798-y.

Abstract

Background: The dysregulation of microRNAs (miRNAs) has been found in diseases and cancers, including microRNA-192 (miR-192). This study was designed to investigate the role of miR-192 in nasopharyngeal carcinoma (NPC) progression.

Methods: The expression levels of miR-192 and some genes were assessed by qRT-PCR and Western blot. The function of miR-192 was investigated through MTT, Transwell, and dual-luciferase reporter assays.

Results: The expression of miR-192 was increased in NPC tissues, and high miR-192 expression predicted poor prognosis in NPC patients. Functionally, upregulation of miR-192 promoted NPC cell migration, invasion, and growth. Furthermore, miR-192 activated EMT and PI3K/AKT pathway to regulate NPC progression. In addition, miR-192 directly targeted RB1 and suppressed its expression in NPC. Moreover, overexpression of RB1 weakened the promoted effect of miR-192 in NPC.

Conclusion: miR-192 promoted cell viability and metastasis in NPC through suppressing RB1 expression and activating PI3K/AKT pathway.

Keywords: Nasopharyngeal carcinoma; PI3K/AKT pathway; RB1; miR-192.

MeSH terms

  • Apoptosis
  • Biomarkers, Tumor / genetics
  • Biomarkers, Tumor / metabolism*
  • Cell Movement
  • Cell Proliferation
  • Epithelial-Mesenchymal Transition
  • Female
  • Follow-Up Studies
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Male
  • MicroRNAs / genetics*
  • Middle Aged
  • Nasopharyngeal Carcinoma / genetics
  • Nasopharyngeal Carcinoma / metabolism
  • Nasopharyngeal Carcinoma / pathology*
  • Nasopharyngeal Neoplasms / genetics
  • Nasopharyngeal Neoplasms / metabolism
  • Nasopharyngeal Neoplasms / pathology*
  • Phosphatidylinositol 3-Kinases / genetics
  • Phosphatidylinositol 3-Kinases / metabolism*
  • Prognosis
  • Proto-Oncogene Proteins c-akt / genetics
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Retinoblastoma Binding Proteins / genetics
  • Retinoblastoma Binding Proteins / metabolism*
  • Signal Transduction
  • Survival Rate
  • Tumor Cells, Cultured
  • Ubiquitin-Protein Ligases / genetics
  • Ubiquitin-Protein Ligases / metabolism*

Substances

  • Biomarkers, Tumor
  • MIRN192 microRNA, human
  • MicroRNAs
  • RB1 protein, human
  • Retinoblastoma Binding Proteins
  • Ubiquitin-Protein Ligases
  • Proto-Oncogene Proteins c-akt