Celecoxib inhibits insulin-like growth factor 1 induced growth and invasion in non-small cell lung cancer

Chen-Hui Liu1, Hong-Guang Bao, Ya-Li Ge

  • 1Departments of Anesthesiology, Affiliated Nanjing Hospital of Nanjing Medical University, Nanjing 210006, P.R. China.

Oncology Letters
|July 9, 2013
PubMed

Insights

Celecoxib hinders non-small cell lung cancer (NSCLC) growth and invasion by impacting the insulin-like growth factor (IGF) axis. This study reveals potential new anticancer mechanisms for celecoxib in NSCLC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Celecoxib is recognized for its role in tumor prevention and treatment.
  • The precise molecular mechanisms underlying celecoxib's anticancer effects remain incompletely understood.
  • The insulin-like growth factor (IGF) axis is implicated in various cancers, including non-small cell lung cancer (NSCLC).

Purpose of the Study:

  • To investigate the impact of celecoxib on insulin-like growth factor 1 (IGF-1)-induced proliferation and invasion in NSCLC cells.
  • To elucidate the molecular pathways through which celecoxib exerts its effects on NSCLC.
  • To explore the modulation of the IGF axis as a potential mechanism for celecoxib's anticancer activity.

Main Methods:

  • A549 NSCLC cells were treated with IGF-1 in the presence or absence of varying concentrations of celecoxib.
  • Cell proliferation and invasion assays were performed to assess cellular responses.
  • Western blot analysis was used to examine the expression of phosphorylated type-1 IGF receptor (IGF-1R) and phosphorylated AKT (p-AKT).
  • Enzyme-linked immunosorbent assay (ELISA) was employed to measure IGF-binding protein-3 (IGFBP-3) levels.

Main Results:

  • Celecoxib demonstrated a dose-dependent inhibition of IGF-1-stimulated cell growth and invasion in A549 cells.
  • Celecoxib treatment led to a reduction in the expression of IGF-1R and IGFBP-3.
  • The phosphorylation of AKT (p-AKT) was decreased following celecoxib administration.
  • These findings indicate that celecoxib interferes with key components of the IGF signaling pathway.

Conclusions:

  • Modulating the IGF axis represents a potential novel mechanism for the anticancer effects of celecoxib in NSCLC.
  • Celecoxib's ability to inhibit IGF-1-induced growth and invasion highlights its therapeutic potential in NSCLC.
  • Further research into the IGF axis may uncover new therapeutic strategies involving celecoxib for NSCLC treatment.

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