title: Inhibition of tumor progression during allergic airway inflammation in a murine model: significant role of TGF-β.
abstract: BACKGROUND
  TGF-β is an important mediator of pulmonary allergic inflammation, and it has been recently reported to be a potential inhibitor of lung tumor progression. The correlation between cancer and allergic inflammatory diseases remains controversial. Thus, the aim of the present study was to evaluate the effects of pulmonary allergic inflammation and in particular the role of TGF-β on cancer progression.
  
  
  METHODS
  Cancer cells were implanted in a BALB/c mice model of allergic airway inflammation, and tumor growth was measured. Apoptosis was evaluated by TUNEL assay, and TGF-β was measured by ELISA. Expression of proliferating cell nuclear antigen, TGF-β, TGF-β receptors I and II, phospho-Smad2 and phospho-Smad4 was evaluated by immunohistochemistry and quantified using digital pathology. The effect of a TGF-β activity inhibitor and recombinant TGF-β on tumor growth was analyzed. The effect of exogenous TGF-β on cell proliferation and apoptosis was evaluated in vitro.
  
  
  RESULTS
  Mice with allergic airway inflammation exhibited decreased tumor volumes due to cell proliferation inhibition and increased apoptosis. TGF-β was increased in the sera and tumor tissues of allergic mice. TGF-β activity inhibition increased tumor progression in allergic mice by enhancing proliferation and decreasing apoptosis of tumor cells. The administration of TGF-β resulted in reduced tumor growth.
  
  
  CONCLUSIONS
  This study is the first to establish an inverse relationship between allergic airway inflammation and tumor progression. This effect appears to be mediated by TGF-β, which is overexpressed in tumor cells during pulmonary allergic inflammation. This study indicates that TGF-β is a potential target for antitumor therapy.
authors.affiliation: Unidad de Investigación en Enfermedades Oncológicas, Hospital Infantil de México Federico Gómez, Dr. Márquez No 262, Col. Doctores, Delegación Cuauhtémoc, C.P. 06720, Mexico City, Mexico.
authors.forename: Belen
authors.initials: B
authors.lastname: Tirado-Rodriguez
authors.forename: Guillermina
authors.initials: G
authors.lastname: Baay-Guzman
authors.forename: Rogelio
authors.initials: R
authors.lastname: Hernandez-Pando
authors.forename: Gabriela
authors.initials: G
authors.lastname: Antonio-Andres
authors.forename: Mario I
authors.initials: MI
authors.lastname: Vega
authors.forename: Leticia
authors.initials: L
authors.lastname: Rocha-Zavaleta
authors.forename: Laura C
authors.initials: LC
authors.lastname: Bonifaz
authors.forename: Sara
authors.initials: S
authors.lastname: Huerta-Yepez
mesh_terms: D000485:Allergens / Q000276:immunology; D000818:Animals; D048708:Cell Growth Processes / Q000276:immunology; D004195:Disease Models, Animal; D018450:Disease Progression; D005260:Female; D008325:Mammary Neoplasms, Experimental / Q000276:immunology* / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D012130:Respiratory Hypersensitivity / Q000276:immunology*; D012137:Respiratory System / Q000382:microbiology*; D015398:Signal Transduction; D016212:Transforming Growth Factor beta / Q000276:immunology*
chemical_list: D000485:Allergens; D016212:Transforming Growth Factor beta