Subject(s)
Helicobacter Infections/complications , Helicobacter pylori , Interleukin-12/genetics , Polymorphism, Single Nucleotide , Protein Subunits/genetics , Stomach Neoplasms/genetics , Adenocarcinoma/genetics , Adult , Aged , Aged, 80 and over , Female , Genetic Predisposition to Disease , Humans , Interleukin-12 Subunit p35 , Interleukin-12 Subunit p40 , Male , Middle Aged , Minisatellite RepeatsABSTRACT
BACKGROUND: We investigated in vitro whether IL-1beta and TGF-beta1 affect pancreatic cancer cell growth, adhesion to the extracellular matrix and Matrigel invasion. MATERIALS AND METHODS: Adhesion to fibronectin, laminin and type I collagen, and Matrigel invasion after stimulation with saline, IL-1beta and TGF-beta1 were evaluated using three primary and three metastatic pancreatic cancer cell lines. RESULTS: Extracellular matrix adhesion of control cells varied independently of the metastatic characteristics of the studied cell lines, whereas Matrigel invasion of control cells was partly correlated with the in vivo metastatic potential. IL-1beta did not influence extracellular matrix adhesion, whereas it significantly enhanced the invasiveness of three of the six cell lines. TGF-beta1 affected the adhesion of one cell line, and exerted contrasting effects on Matrigel invasion of different cell lines. CONCLUSIONS: IL-1beta enhances the invasive capacity of pancreatic cancer cells, whereas TGF-beta1 has paradoxical effects on pancreatic cancer cells; this makes it difficult to interfere with TGF-beta1 signaling in pancreatic cancer treatment.
