endotoxin induces proliferation of nsclc in vitro and in vivo role of cox2 and egfr activation lung cancer is frequently complicated by pulmonary infections which may impair prognosis of this disease therefore we investigated the effect of bacterial lipopolysaccharides lps on tumor proliferation in vitro in the nonsmall cell lung cancer nsclc cell line a549 ex vivo in a tissue culture model using human nsclc specimens and in vivo in the a549 adenocarcinoma mouse model lps induced a time and dosedependent increase in proliferation of a549 cells as quantified by mts activity and cell counting in parallel an increased expression of the proliferation marker ki67 and cyclooxygenase cox2 was detected both in a549 cells and in ex vivo human nsclc tissue large amounts of cox2derived prostaglandin pge2 were secreted from lpsstimulated a549 cells pharmacological interventions revealed that the proliferative effect of lps was dependent on cd14 and tolllike receptor tlr4 moreover blocking of the epidermal growth factor receptor egfr also decreased lpsinduced proliferation of a549 cells inhibition of cox2 activity in a549 cells severely attenuated both pge2 release and proliferation in response to lps synthesis of pge2 was also reduced by inhibiting cd14 tlr4 and egfr in a549 cells the proliferative effect of lps on a549 cells could be reproduced in the a549 adenocarcinoma mouse model with enhancement of tumor growth and ki67 expression in implanted tumors in summary lps induces proliferation of nsclc cells in vitro ex vivo in human nsclc specimen and in vivo in a mouse model of nsclc pulmonary infection may thus directly induce tumor progression in nsclc