OBJECTIVES: Trefoil factor family (TFF) peptides promote wound healing in the gut. Recent evidence has suggested that TFF3 may be a pancreatic mitogen, an unusual role for TFF peptides. We sought to clarify human pancreatic TFF and mucin expression and performed in vitro experiments to see how pancreatic cell lines respond to TFF3 in particular. METHODS: Samples of normal and diseased pancreas (chronic pancreatitis, pancreatic intraepithelial neoplasia, neuroendocrine tumors, and pancreatic ductal adenocarcinoma [PDAC]) were studied by immunohistochemistry and in situ hybridization. Pancreatic cell lines were challenged with TFF2 and TFF3 in wound and migration assays. RESULTS: In normal islets, colocalization of insulin or glucagon with TFF3 was common. All TFF messenger RNAs were seen in ductal epithelium. Adenocarcinomas expressed all TFF messenger RNAs. Normal ducts were mucin free; MUC5AC was strongest in pancreatic intraepithelial neoplasia and chronic pancreatitis but was reduced in PDAC. TFF2 induced Panc-1 migration and accelerated wound closure in Capan-2 and COLO-357. Double immunohistochemistry for insulin or TFF3 and Ki67 colabeled only very rare islet cells. TFF3-positive PDAC ducts showed some Ki67 colocalization. CONCLUSIONS: No correlation between TFF3 or insulin and Ki67 was seen without ductal hyperplasia. TFF2 may assist pancreatic tumor cell movement, but TFF3 may not be a pancreatic mitogen.
OBJECTIVES: Trefoil factor family (TFF) peptides promote wound healing in the gut. Recent evidence has suggested that TFF3 may be a pancreatic mitogen, an unusual role for TFF peptides. We sought to clarify humanpancreatic TFF and mucin expression and performed in vitro experiments to see how pancreatic cell lines respond to TFF3 in particular. METHODS: Samples of normal and diseased pancreas (chronic pancreatitis, pancreatic intraepithelial neoplasia, neuroendocrine tumors, and pancreatic ductal adenocarcinoma [PDAC]) were studied by immunohistochemistry and in situ hybridization. Pancreatic cell lines were challenged with TFF2 and TFF3 in wound and migration assays. RESULTS: In normal islets, colocalization of insulin or glucagon with TFF3 was common. All TFF messenger RNAs were seen in ductal epithelium. Adenocarcinomas expressed all TFF messenger RNAs. Normal ducts were mucin free; MUC5AC was strongest in pancreatic intraepithelial neoplasia and chronic pancreatitis but was reduced in PDAC. TFF2 induced Panc-1 migration and accelerated wound closure in Capan-2 and COLO-357. Double immunohistochemistry for insulin or TFF3 and Ki67 colabeled only very rare islet cells. TFF3-positive PDAC ducts showed some Ki67 colocalization. CONCLUSIONS: No correlation between TFF3 or insulin and Ki67 was seen without ductal hyperplasia. TFF2 may assist pancreatic tumor cell movement, but TFF3 may not be a pancreatic mitogen.
Authors: Rahat Jahan; Koelina Ganguly; Lynette M Smith; Pranita Atri; Joseph Carmicheal; Yuri Sheinin; Satyanarayana Rachagani; Gopalakrishnan Natarajan; Randall E Brand; Muzafar A Macha; Paul M Grandgenett; Sukhwinder Kaur; Surinder K Batra Journal: EBioMedicine Date: 2019-04-05 Impact factor: 8.143
Authors: Nayara Braga Emidio; Rajeshwari Meli; Hue N T Tran; Hayeon Baik; Séverine Morisset-Lopez; Alysha G Elliott; Mark A T Blaskovich; Sabrina Spiller; Annette G Beck-Sickinger; Christina I Schroeder; Markus Muttenthaler Journal: J Med Chem Date: 2021-06-18 Impact factor: 7.446
Authors: George Pentheroudakis; Vassiliki Kotoula; Elena Fountzilas; George Kouvatseas; George Basdanis; Ioannis Xanthakis; Thomas Makatsoris; Elpida Charalambous; Demetris Papamichael; Epaminontas Samantas; Pavlos Papakostas; Dimitrios Bafaloukos; Evangelia Razis; Christos Christodoulou; Ioannis Varthalitis; Nicholas Pavlidis; George Fountzilas Journal: BMC Cancer Date: 2014-02-20 Impact factor: 4.430