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World J Gastroenterol. Aug 7, 2014; 20(29): 10038-10049
Published online Aug 7, 2014. doi: 10.3748/wjg.v20.i29.10038
Published online Aug 7, 2014. doi: 10.3748/wjg.v20.i29.10038
Aspirin inhibits cell viability and mTOR downstream signaling in gastroenteropancreatic and bronchopulmonary neuroendocrine tumor cells
Matilde Spampatti, George Vlotides, Gerald Spöttl, Julian Maurer, Burkhard Göke, Christoph J Auernhammer, Department of Internal Medicine II, University-Hospital Campus Grosshadern, Interdisciplinary Center of Neuroendocrine Tumours of the GastroEnteroPancreatic System (GEPNET-KUM), Ludwig-Maximilians-University of Munich, 81377 Munich, Germany
Matilde Spampatti, U.O.C.Gastroenterologia 2 Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico, Università degli Studi di Milano, 20122 Milano, Italy
Author contributions: Spampatti M and Vlotides G contributed equally to this work; Spampatti M, Vlotides G and Auernhammer CJ designed the research, Spampatti M, Spöttl G and Maurer J performed the research; Göke B contributed new reagents and analytic tools; Spampatti M, Vlotides G, Göke B and Auernhammer CJ wrote the paper.
Correspondence to: Dr. Christoph J Auernhammer, Department of Internal Medicine II, University-Hospital Campus Grosshadern, Interdisciplinary Center of Neuroendocrine Tumours of the GastroEnteroPancreatic System (GEPNET-KUM), Ludwig-Maximilians-University of Munich, Marchioninistr 15, 81377 Munich, Germany. cauernha@med.uni-muenchen.de
Telephone: +49-89-440072520 Fax: +49-89-440075514
Received: June 18, 2013
Revised: January 8, 2014
Accepted: January 20, 2014
Published online: August 7, 2014
Revised: January 8, 2014
Accepted: January 20, 2014
Published online: August 7, 2014
Core Tip
Core tip: We evaluated the effects of aspirin on pancreatic (BON1), bronchopulmonary (NCI-H727) and midgut (GOT1) neuroendocrine tumor cell lines and demonstrated that aspirin has potent antitumor properties in vitro. Aspirin caused a dose-dependent reduction of cell viability/cell proliferation, the inhibition of targets downstream of mammalian target of rapamycin and the (compensatory) activation of the AKT and extracellular signal-regulated kinase signaling pathways. Treatment of BON1 and NCI-H727 cells with aspirin reduced the entry of these cells into the S phase of the cell cycle, and this effect was associated with the induction of p21 and reduced cyclin-dependent kinase 4 and cyclin D3 expression.