Inhibition of tumor progression during allergic airway inflammation in a murine model: significant role of TGF-β View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-06-16

AUTHORS

Belen Tirado-Rodriguez, Guillermina Baay-Guzman, Rogelio Hernandez-Pando, Gabriela Antonio-Andres, Mario I. Vega, Leticia Rocha-Zavaleta, Laura C. Bonifaz, Sara Huerta-Yepez

ABSTRACT

INTRODUCTION: 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. CONCLUSION: 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. More... »

PAGES

1205-1214

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00262-015-1722-4

DOI

http://dx.doi.org/10.1007/s00262-015-1722-4

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1030275824

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/26076663


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28 schema:description INTRODUCTION: 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. CONCLUSION: 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.
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35 schema:keywords BALB/c mouse model
36 ELISA
37 TGF
38 TUNEL
39 activity inhibition
40 activity inhibitor
41 administration
42 administration of TGF
43 aim
44 airway inflammation
45 allergic airway inflammation
46 allergic inflammation
47 allergic inflammatory diseases
48 allergic mice
49 antigen
50 antitumor therapy
51 apoptosis
52 c mice model
53 cancer
54 cancer cells
55 cancer progression
56 cell nuclear antigen
57 cell proliferation
58 cell proliferation inhibition
59 cells
60 correlation
61 digital pathology
62 disease
63 effect
64 exogenous TGF
65 expression
66 growth
67 immunohistochemistry
68 important mediator
69 inflammation
70 inflammatory diseases
71 inhibition
72 inhibitors
73 inverse relationship
74 lung tumor progression
75 mediators
76 mice
77 model
78 mouse model
79 murine model
80 nuclear antigen
81 pathology
82 phospho-Smad2
83 phospho-Smad4
84 potential inhibitors
85 potential target
86 present study
87 progression
88 proliferation
89 proliferation inhibition
90 pulmonary allergic inflammation
91 receptor I
92 recombinant TGF
93 reduced tumor growth
94 relationship
95 role
96 role of TGF
97 serum
98 significant role
99 study
100 target
101 therapy
102 tissue
103 tumor cells
104 tumor growth
105 tumor progression
106 tumor tissue
107 tumor volume
108 volume
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