title: Cytokines may influence tumor growth and spread. An in vitro study in two human cancer cell lines.
abstract: Tumor spread may be favored by a reduced production and/or an enhanced degradation of extracellular matrix components (collagen, fibronectin, laminin). Most tumor cell behavior, from growth to spread, may be regulated by cytokines, the exact roles of which, however, are not yet fully understood. We here evaluate the effects of some cytokines (epidermal growth factor, transforming growth factor-beta 1, interleukin-1 alpha, and interleukin-1 beta) on both cell growth and the production of the aminoterminal peptide of type III procollagen, the urokinase plasminogen activator, and the plasminogen activator inhibitor-1 in neoplastic cell lines originating in the pancreas and colon. Cells were stimulated daily with the above cytokines and the aminoterminal peptide of type III procollagen, urokinase plasminogen activator, and plasminogen activator inhibitor-1 were measured in the conditioned media. Epidermal growth factor stimulated cell growth of both cell lines. Transforming growth factor-beta 1 counteracted cell proliferation and stimulated type III procollagen and plasminogen activator inhibitor-1 production only in the colon cancer cell line. Interleukin-1 alpha slightly stimulated cell growth, but inhibited plasminogen activator inhibitor-1 production in both cell lines; interleukin-1 beta did not affect cell growth, but stimulated plasminogen activator inhibitor-1 production by the colon cancer cell line. Our findings suggest that transforming growth factor-beta 1 and interleukin-1 beta may have an antidiffusive effect. These results confirm that cytokine-producing cells have a potential role in stimulating or counteracting tumor growth and spread and also confirm the pivotal role of host-tumor interactions in determining the outcome of a particular neoplasia.
authors.affiliation: Department of Laboratory Medicine, University of Padua, Italy.
authors.forename: M P
authors.initials: MP
authors.lastname: Panozzo
authors.forename: D
authors.initials: D
authors.lastname: Basso
authors.forename: M
authors.initials: M
authors.lastname: De Paoli
authors.forename: P
authors.initials: P
authors.lastname: Carraro
authors.forename: D
authors.initials: D
authors.lastname: Burighel
authors.forename: M
authors.initials: M
authors.lastname: Plebani
mesh_terms: D002455:Cell Division / Q000187:drug effects; D003094:Collagen / Q000378:metabolism; D003110:Colonic Neoplasms / Q000378:metabolism / Q000473:pathology*; D016207:Cytokines / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004815:Epidermal Growth Factor / Q000494:pharmacology; D006801:Humans; D007375:Interleukin-1 / Q000494:pharmacology; D010190:Pancreatic Neoplasms / Q000378:metabolism / Q000473:pathology*; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism; D015842:Serine Proteinase Inhibitors / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000494:pharmacology; D014407:Tumor Cells, Cultured; D014568:Urokinase-Type Plasminogen Activator / Q000378:metabolism
chemical_list: D016207:Cytokines; D007375:Interleukin-1; D017395:Plasminogen Activator Inhibitor 1; D015842:Serine Proteinase Inhibitors; D016212:Transforming Growth Factor beta; D004815:Epidermal Growth Factor; D003094:Collagen; D014568:Urokinase-Type Plasminogen Activator