MicroRNA-107-5p suppresses non-small cell lung cancer by directly targeting oncogene epidermal growth factor receptor

Ping Wang1, Xiaomin Liu1, Yang Shao1,2

  • 1Laboratory for Noncoding RNA & Cancer, School of Life Sciences, Shanghai University, Shanghai, China.

Oncotarget
|September 17, 2017
PubMed

Insights

MicroRNA-107-5p (miR-107-5p) is decreased in non-small cell lung cancer (NSCLC). This microRNA suppresses tumor growth, proliferation, and metastasis by targeting the epidermal growth factor receptor (EGFR).

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • MicroRNAs (miRNAs) are crucial regulators of gene expression, and their dysregulation is implicated in various cancers, including non-small cell lung cancer (NSCLC).
  • The specific role of microRNA-107-5p (miR-107-5p) in the pathogenesis and progression of NSCLC remains incompletely understood.
  • Epidermal growth factor receptor (EGFR) is a key oncogene driving tumorigenesis in several cancer types.

Purpose of the Study:

  • To investigate the expression levels of miR-107-5p in NSCLC tissues and cell lines.
  • To elucidate the functional role of miR-107-5p in NSCLC progression, including its effects on cell proliferation, metastasis, cell cycle, and apoptosis.
  • To determine if miR-107-5p directly targets EGFR and to evaluate its therapeutic potential in NSCLC.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) was used to measure miR-107-5p expression in NSCLC tissues and cell lines.
  • Functional assays were performed to assess the impact of miR-107-5p on cell proliferation, migration, invasion, cell cycle progression, and apoptosis.
  • Bioinformatic analysis and luciferase reporter assays were employed to validate EGFR as a direct target of miR-107-5p.
  • In vivo studies using animal models were conducted to evaluate the effect of miR-107-5p on tumor growth.

Main Results:

  • miR-107-5p expression was found to be significantly downregulated in NSCLC tissues and cell lines compared to normal controls.
  • Overexpression of miR-107-5p suppressed NSCLC cell proliferation, inhibited metastasis, impeded cell cycle progression, and promoted apoptosis.
  • EGFR was identified as a direct target of miR-107-5p, and its expression was inversely correlated with miR-107-5p levels.
  • In vivo experiments demonstrated that miR-107-5p administration inhibited tumor growth in NSCLC models.

Conclusions:

  • miR-107-5p acts as a tumor suppressor in NSCLC by directly targeting and inhibiting the expression of EGFR.
  • Restoration of miR-107-5p levels can impede NSCLC progression and inhibit tumor growth.
  • miR-107-5p represents a promising novel therapeutic target for the treatment of lung cancer.

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