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FOXM1 promotes the progression of non-small cell lung cancer by inhibiting miR-509-5p expression via binding to the

Mengcha Tian1, Jiaming Li1, Huihui Wu1

  • 1Department of Clinical Laboratory, Quanzhou First Hospital Affiliated to Fujian Medical University, Quanzhou, 362000, China.

Heliyon
|March 18, 2024
PubMed
Summary

Forkhead box M1 (FOXM1) promotes non-small cell lung cancer by inhibiting miR-509-5p. Inhibiting FOXM1 with FDI-6 suppressed cancer progression and increased miR-509-5p, offering potential therapeutic strategies.

Keywords:
FOXM1InhibitorsNon-small cell carcinomaPromotermiR-509-5p

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Area of Science:

  • Molecular biology
  • Cancer research
  • Gene regulation

Background:

  • Forkhead box M1 (FOXM1) is a transcription factor overexpressed in multiple cancers, including non-small cell lung cancer (NSCLC).
  • FOXM1 overexpression correlates with poor prognosis in NSCLC patients, but its precise role in NSCLC development is not fully understood.

Purpose of the Study:

  • To investigate the mechanism by which FOXM1 influences lung cancer cell migration, invasion, apoptosis, and viability.
  • To elucidate the regulatory relationship between FOXM1 and miR-509-5p in NSCLC.

Main Methods:

  • Utilized Transwell assays, scratch tests, and flow cytometry to assess FOXM1's impact on A549 lung cancer cell behavior.
  • Employed quantitative PCR, dual-luciferase reporter assays, and chromatin immunoprecipitation to determine FOXM1's effect on miR-509-5p expression and its binding mechanism.

Main Results:

  • Inhibition of FOXM1 using FDI-6 decreased FOXM1 protein levels, upregulated miR-509-5p, and reduced NSCLC cell migration, invasion, and viability while promoting apoptosis.
  • Administration of a miR-509-5p inhibitor counteracted the effects of FDI-6, indicating FOXM1's cancer-promoting role is mediated through miR-509-5p.
  • FOXM1 was found to directly bind to the miR-509-5p promoter, inhibiting its expression.

Conclusions:

  • FOXM1 directly suppresses miR-509-5p expression by binding to its promoter, establishing a negative feedback loop that promotes NSCLC development.
  • These findings provide insights into NSCLC pathogenesis and identify FOXM1 and miR-509-5p as potential therapeutic targets for NSCLC treatment.