AI Article Synopsis

  • Celecoxib has potential anticancer effects in non-small cell lung cancer (NSCLC) by inhibiting IGF-1-induced growth and invasion.
  • The study analyzed how celecoxib affects the expression of key proteins involved in the IGF pathway, specifically IGF-1 receptor and AKT phosphorylation.
  • Results showed that celecoxib reduced these proteins' expressions and was effective in a dose-dependent manner, indicating a new mechanism for its anticancer properties.

Article Abstract

Despite a large number of studies indicating that celecoxib plays an important role in the prevention and treatment of tumors, the detailed molecular mechanisms are not well understood. The aim of the present study was to investigate the effect of celecoxib on insulin-like growth factor 1 (IGF-1)-induced growth and invasion in non-small cell lung cancer (NSCLC). For these experiments, IGF-1-induced cell growth and invasion were analyzed in A549 cells in the presence and absence of celecoxib. The effects of celecoxib on the expression of phosphorylated type-1 IGF receptor (IGF-1R) and phosphorylated AKT (p-AKT) were examined using western blot analysis. The influence of celecoxib on IGF-binding protein-3 (IGFBP-3) expression was analyzed using ELISA. Celecoxib inhibited IGF-1-stimulated growth and invasion in a dose-dependent manner. Celecoxib also reduced the expression of IGF-1R, IGFBP-3 and phosphorylation of AKT. The results suggest that modulating the IGF axis may be a new mechanism for the anticancer effect of celecoxib on NSCLC.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3701083PMC
http://dx.doi.org/10.3892/ol.2013.1277DOI Listing

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