miR-675 promotes disease progression of non-small cell lung cancer via activating NF-κB signaling pathway

Cell Mol Biol (Noisy-le-grand). 2017 May 20;63(5):7-10. doi: 10.14715/cmb/2017.63.5.2.

Abstract

Non-small cell lung cancer (NSCLC) is a major type of lung cancer significantly affected human life. Current studies have revealed potential role of miR-675 in the etiology of lung cancer. Therefore, in this study, we aimed to investigate the role of miR-675 in NSCLC cell line. We recruited 92 cases of NSCLC patients from July 2009 to February 2011 in the oncology department. Tumor and peripheral tissue was collected for miR-675 expression. NSCLC cell lines with either miR-675 over-expression or low-expression were established. Western blotting and immunofluorescence staining were used for detecting P65 and pP65 expression and translocation in the nuclei. MiR-675 expression was significantly higher in the lung cancer tissue than the peripheral normal tissue (P < 0.001). The gene expression of pP65 was also increased and decreased in cells with over-expression or low-expression of miR-675, respectively (both P < 0.05). Whereas the trend of P65 expression was on the opposite (both P < 0.05), indicating the NF-κB signaling pathway was activated when miR-675 was expressed and vice versa. Immunofluorescence staining showed that more pP65 expression was clustered in the nuclei in miR-675 over-expressed cells, which further demonstrated NF-κB signaling pathway activation. Increased miR-675 expression is associated with NSCLC progression through activation of NF-κB signaling pathway.

Keywords: NF-κB; Non-small cell lung cancer.; miR-675.

MeSH terms

  • A549 Cells
  • Carcinoma, Non-Small-Cell Lung / genetics*
  • Carcinoma, Non-Small-Cell Lung / pathology*
  • Cell Nucleus / metabolism
  • Disease Progression*
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Lung Neoplasms / genetics*
  • Lung Neoplasms / pathology*
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • NF-kappa B / metabolism*
  • Protein Transport
  • Signal Transduction*
  • Transcription Factor RelA / metabolism

Substances

  • MIRN675 microRNA, human
  • MicroRNAs
  • NF-kappa B
  • RELA protein, human
  • Transcription Factor RelA