RT Journal Article SR Electronic T1 Loss of polymeric immunoglobulin receptor expression is associated with lung tumorigenesis JF European Respiratory Journal JO Eur Respir J FD European Respiratory Society SP erj01844-2010 DO 10.1183/09031936.00184410 A1 S. Ocak A1 T.V. Pedchenko A1 H. Chen A1 F.T. Harris A1 J. Qian A1 V. Polosukhin A1 C. Pilette A1 Y. Sibille A1 A.L. Gonzalez A1 P.P. Massion YR 2011 UL http://erj.ersjournals.com/content/early/2011/09/29/09031936.00184410.abstract AB Polymeric immunoglobulin receptor (pIgR) expression is downregulated in lung cancer, but implications in lung tumorigenesis remain unknown. We hypothesized that loss of pIgR expression occurs early, is associated with cell proliferation and poor prognosis.pIgR expression was evaluated by immunohistochemistry in airways of patients with normal mucosa, preinvasive and invasive lesions and correlated with clinical outcomes. 16-HBE and A549 cells stably transfected with pIgR were tested for proliferation, apoptosis and cell cycle.Immunostaining was strong in normal epithelium, but severely reduced in preinvasive lesions and most lung cancers. Persistent expression was associated with younger age and adenocarcinoma subtype but not survival. pIgR overexpression significantly reduced A549 and 16-HBE proliferation. Growth inhibition was not due to cell cycle arrest, increased apoptosis or endoplasmic reticulum stress but we observed altered expression of genes encoding for membrane proteins, including NOTCH3. Interestingly, NOTCH3 expression was inversely correlated with pIgR expression in cell lines and tissues.pIgR expression was lost in most lung cancers and preinvasive bronchial lesions, suggesting that pIgR downregulation is an early event in lung tumorigenesis. pIgR overexpression in A549 and 16-HBE inhibited proliferation. Future investigations are required to determine mechanisms by which pIgR contributes to cell proliferation.