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miR-150, p53 protein and relevant miRNAs consist of a regulatory network in NSCLC tumorigenesis

De-Tao Wang1, Zhong-Liang Ma, Yan-Li Li

  • 1School of Life Sciences, Shanghai University, Shanghai 200444, P.R. China.

Oncology Reports
|May 15, 2013
PubMed

Insights

MicroRNA-150 (miR-150) targets tumor protein p53 in non-small cell lung cancer (NSCLC), downregulating its expression and influencing cell cycle progression. This reveals a regulatory network involving miR-150, p53, and other microRNAs in NSCLC.

Area of Science:

  • Molecular Biology
  • Oncology
  • Gene Regulation

Background:

  • MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression post-transcriptionally.
  • Tumor protein p53 is a critical transcription factor involved in tumorigenesis.
  • Understanding miRNA-p53 interactions is crucial for non-small cell lung cancer (NSCLC) research.

Purpose of the Study:

  • To investigate the functional role of miR-150 and p53 in non-small cell lung cancer (NSCLC).
  • To determine if miR-150 directly targets the 3'-untranslated region (3'-UTR) of p53.
  • To explore the impact of miR-150 and p53 on cell cycle progression and identify p53-regulated miRNAs.

Main Methods:

  • Construction of expression vectors for p53 and its 3'-UTR, and reporter vectors for luciferase assays.
  • Transfection with miR-150 mimics and miRNA-negative control (miRNA-NC) to assess p53 downregulation and luciferase activity.
  • Quantitative real-time PCR (qRT-PCR) to analyze the expression of miR-150, p53, and other miRNAs in NSCLC tissues and cell lines.

Main Results:

  • miR-150 mimics significantly reduced luciferase activity and downregulated p53 protein expression by targeting the p53 3'-UTR.
  • Expression levels of miR-150 were higher in T2 stage NSCLC tissues compared to T1 stage, with a corresponding correlation to p53 expression.
  • p53 transfection induced G1 phase arrest, while co-transfection with miR-150 mimics and p53 3'-UTR reporter vectors reduced G1 phase percentage. p53 upregulated miR-34a, miR-184, miR-181a, and miR-148.

Conclusions:

  • miR-150 directly targets the 3'-UTR of p53, leading to its downregulation in NSCLC.
  • p53 protein positively regulates the expression of specific miRNAs (miR-34a, miR-184, miR-181a, miR-148) that influence cell cycle progression.
  • These findings establish a regulatory network involving miR-150, p53, and associated miRNAs in the context of NSCLC tumorigenesis.

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