ECE2015 Eposter Presentations Reproduction, endocrine disruptors and signalling (92 abstracts)
Role of TGFβ1 in pancreatic neuroendocrine tumour
Simona Falletta 1 , Teresa Gagliano 1 , Erica Gentilin 1 , Carmelina Di Pasquale 1 , Katiuscia Benfini 1 , Vanessa Polenta 2 , Massimo Falconi 2 , Maria Rosaria Ambrosio 2 , Stefano Partelli 2 , Ettore degli Uberti 1 & Maria Chiara Zatelli 1
1Section of Endocrinology and Internal Medicine, Department of Medical Science, University of Ferrara, Italy, Ferrara, Italy; 2Pancreatic Surgery Unit, San Raffaele Hospital, Vita-Salute San Raffaele University, Via Olgettina 60, 20132 Milan, Italy.
Introduction: Neuroendocrine tumours (NETs) are heterogeneous neoplasms arising from neuroendocrine cells spread in the respiratory and gastro-entero-pancreatic epithelium. The role of transforming growth factor beta-1 (TGFβ1) in NET biology is largely unknown. TGFβ1 signalling pathway is tumour suppressive in most non-transformed epithelial cell lines. In contrast, many human carcinomas are refractory to the growth–inhibitory effects of TGFβ1.
Aim: To understand the possible role of TGFβ1 on cell viability and apoptosis in pNET and to evaluate whether this protein may affect the response to therapeutic molecules currently used in the management of pNETs.
Methods: 20 pNETs primary cultures were treated with TGFβ1 and/or everolimus, a mTOR inhibitor. Cell viability and caspase activity were evaluated.
Results: TGFβ1 reduced cell viability and promoted apoptosis (~50%) in four pNETs. In the same group, TGFβ1 enhanced (+15%) the growth arrest induced by everolimus alone (50%). On the contrary in 16 pNETs we observed a 30% increase in cell viability and a similar decrease in caspase activation.
Conclusions: In conclusion, TGFβ1 reduces cell viability in a pNET sub-group and may cooperate with everolimus. Further studies are necessary to understand TGFβ1 related functional context in pNETs.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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