MiR-183-5p is required for non-small cell lung cancer progression by repressing PTEN

Biomed Pharmacother. 2019 Mar:111:1103-1111. doi: 10.1016/j.biopha.2018.12.115. Epub 2019 Jan 11.

Abstract

Lung cancer is the leading cause in all cancer deaths. A low survival rate and high recurrence rate of lung cancer make the endeavor to identify new, more effective therapies a primary goal. MicroRNAs (miRNAs) are regarded as regulators of tumorigenesis and it is known that miR-183-5p is significantly upregulated in non-small cell lung cancer (NSCLC), suggesting it has an oncogenic function in lung cancer. In this study, we found that miR-183-5p could promote lung carcinogenesis by directly targeting phosphatase tensin (PTEN). Further experiments indicated that miR-183-5p could suppress p53 and activate AKT signaling through phosphorylation. Moreover, our data indicated that miR-183-5p promoted tumor metastasis and tumor growth in vivo. Collectively, these results showed that miR-183-5p is required for NSCLC development through the suppressing PTEN, and might be a promising target in the diagnosis and treatment of lung cancer in the future.

Keywords: Non-small cell lung cancer; PTEN; Tumorigenesis; miR-183-5p.

MeSH terms

  • A549 Cells
  • Aged
  • Animals
  • Carcinogenesis / genetics
  • Carcinoma, Non-Small-Cell Lung / genetics*
  • Cell Line, Tumor
  • Cell Proliferation / genetics
  • Female
  • Gene Expression Regulation, Neoplastic / genetics
  • Humans
  • Lung Neoplasms / genetics*
  • Mice
  • Mice, Nude
  • MicroRNAs / genetics*
  • Middle Aged
  • PTEN Phosphohydrolase / genetics*
  • Proto-Oncogene Proteins c-akt / genetics
  • Signal Transduction / genetics
  • Up-Regulation / genetics

Substances

  • MIRN183 microRNA, human
  • MicroRNAs
  • Proto-Oncogene Proteins c-akt
  • PTEN Phosphohydrolase
  • PTEN protein, human