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Background  Cyclooxygenase‐2‐derived prostaglandin  E 2   ( PGE 2  ) stimulates tumor cell growth and progression. α7 nicotinic acetylcholine receptor ( nAChR ) is a major mediator of cholinergic signaling in tumor cells. In the present study, we investigated the mechanisms by which  PGE 2   increases non‐small cell lung cancer ( NSCLC ) proliferation via α7  nAChR  induction.    Methods  The effects of  PGE 2   on α7  nAChR  expression, promoter activity, and cell signaling pathways were detected by  W estern blot analysis, real time reverse transcriptase polymerase chain reaction, and transient transfection assay. The effect of  PGE 2   on cell growth was determined by cell viability assay.    Results  We found that  PGE 2   induced α7  nAChR  expression and its promoter activity in  NSCLC  cells. The stimulatory role of  PGE 2   on cell proliferation was attenuated by α7  nAChR  small interfering ribonucleic acids (si RNA ) or acetylcholinesterase.  PGE 2  ‐induced α7  nAChR  expression was blocked by an antagonist of the  PGE 2   receptor subtype  EP 4 and by  EP 4 si RNA . Furthermore,  PGE 2   enhanced α7  nAChR  expression via activation of c‐ J un  N ‐terminal kinase ( JNK ), phosphatidylinositol 3‐kinase ( PI3‐K ), and protein kinase  A  ( PKA ) pathways followed by increased c‐Jun expression, a critical transcription factor. Blockade of c‐ J un diminished the effects of  PGE 2   on α7  nAChR  promoter activity and protein expression, and cell growth.    Conclusion  Our results demonstrate that  PGE 2   promotes  NSCLC  cell growth through increased α7  nAChR  expression. This effect is dependent on  EP 4‐mediated activation of  JNK ,  PI3K,  and  PKA  signals that induce c‐Jun protein expression and α7  nAChR  gene promoter activity. Our findings unveil a novel link between prostanoids and cholinergic signaling.

thoracic cancer

Novel link between prostaglandin E 2  ( PGE 2  ) and cholinergic signaling in lung cancer: The role of c‐ J un in  PGE 2  ‐induced α7 nicotinic acetylcholine receptor expression and tumor cell proliferation