Interferon-Gamma and Tumor Necrosis Factor-Related Weak Inducer of Apoptosis Expression in Neoangiogenesis in Colorectal Polypoid Lesions.


Journal

European surgical research. Europaische chirurgische Forschung. Recherches chirurgicales europeennes
ISSN: 1421-9921
Titre abrégé: Eur Surg Res
Pays: Switzerland
ID NLM: 0174752

Informations de publication

Date de publication:
2019
Historique:
received: 05 09 2018
accepted: 19 08 2019
pubmed: 10 10 2019
medline: 19 6 2020
entrez: 10 10 2019
Statut: ppublish

Résumé

Interferon gamma (IFNγ) and tumor necrosis factor-related weak inducer of apoptosis (TWEAK) molecules seem to have a potential effect on angiogenic factors such as vascular endothelial growth factor (VEGF). The aim of this study was to assess a possible interplay between IFNγ and TWEAK cytokines and VEGF machinery in the different steps of colorectal carcinogenesis. A total of 92 subjects with colonic adenoma or cancer who underwent screening colonoscopy or surgery were prospectively enrolled. Polypoid lesion tissue samples were collected and frozen. Real-time reverse transcription polymerase chain reaction for IFNγ, TWEAK, and VEGF-A mRNA expression was performed. Immunoassays for VEGF-A, VEGF-C, VEGFR-1, VEGFR-2, and VEGFR-3 were also performed. Nonparametric statistics, receiver operating characteristic curve analysis, and logistic multiple regression analysis were used. IFNγ and TWEAK mRNA expression was higher in patients with T2 or more advanced colorectal cancer than in those with adenomas or T1 cancer (p < 0.001 and p = 0.01, respectively). IFNγ and TWEAK mRNA expression levels directly correlated with VEGF-A mRNA expression levels (rho = 0.44, p < 0.001 and rho = 0.29, p = 0.004, respectively). On the contrary, IFNγ and TWEAK mRNA expression levels inversely correlated with VEGF-C protein levels (rho = -0.29, p = 0.04 and rho = -0.31, p = 0.03, respectively). Similarly, IFNγ and TWEAK mRNA expression levels inversely correlated with VEGFR2 protein levels (rho = -0.38, p = 0.033 and rho = -0.40, p = 0.025, respectively). This study showed that in colorectal polypoid lesions, IFNγ and TWEAK expressions are directly correlated to VEGF-A expression but inversely correlated with VEGFR2 levels, suggesting a possible feedback mechanism in the regulation of VEGF-A expression.

Sections du résumé

BACKGROUND BACKGROUND
Interferon gamma (IFNγ) and tumor necrosis factor-related weak inducer of apoptosis (TWEAK) molecules seem to have a potential effect on angiogenic factors such as vascular endothelial growth factor (VEGF). The aim of this study was to assess a possible interplay between IFNγ and TWEAK cytokines and VEGF machinery in the different steps of colorectal carcinogenesis.
METHODS METHODS
A total of 92 subjects with colonic adenoma or cancer who underwent screening colonoscopy or surgery were prospectively enrolled. Polypoid lesion tissue samples were collected and frozen. Real-time reverse transcription polymerase chain reaction for IFNγ, TWEAK, and VEGF-A mRNA expression was performed. Immunoassays for VEGF-A, VEGF-C, VEGFR-1, VEGFR-2, and VEGFR-3 were also performed. Nonparametric statistics, receiver operating characteristic curve analysis, and logistic multiple regression analysis were used.
RESULTS RESULTS
IFNγ and TWEAK mRNA expression was higher in patients with T2 or more advanced colorectal cancer than in those with adenomas or T1 cancer (p < 0.001 and p = 0.01, respectively). IFNγ and TWEAK mRNA expression levels directly correlated with VEGF-A mRNA expression levels (rho = 0.44, p < 0.001 and rho = 0.29, p = 0.004, respectively). On the contrary, IFNγ and TWEAK mRNA expression levels inversely correlated with VEGF-C protein levels (rho = -0.29, p = 0.04 and rho = -0.31, p = 0.03, respectively). Similarly, IFNγ and TWEAK mRNA expression levels inversely correlated with VEGFR2 protein levels (rho = -0.38, p = 0.033 and rho = -0.40, p = 0.025, respectively).
CONCLUSION CONCLUSIONS
This study showed that in colorectal polypoid lesions, IFNγ and TWEAK expressions are directly correlated to VEGF-A expression but inversely correlated with VEGFR2 levels, suggesting a possible feedback mechanism in the regulation of VEGF-A expression.

Identifiants

pubmed: 31597147
pii: 000502786
doi: 10.1159/000502786
doi:

Substances chimiques

Cytokine TWEAK 0
RNA, Messenger 0
TNFSF12 protein, human 0
Vascular Endothelial Growth Factor A 0
Interferon-gamma 82115-62-6
KDR protein, human EC 2.7.10.1
Vascular Endothelial Growth Factor Receptor-2 EC 2.7.10.1

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

186-195

Informations de copyright

© 2019 S. Karger AG, Basel.

Auteurs

Cesare Ruffolo (C)

General Surgery Unit, University Hospital of Padova, Padova, Italy.

Luisa Toffolatti (L)

Pathology Unit, Cà Foncello Regional Hospital, Treviso, Italy.

Marco Massani (M)

Department of Surgery, Cà Foncello Regional Hospital, Treviso, Italy.

Anna Pozza (A)

Department of Surgery, Cà Foncello Regional Hospital, Treviso, Italy.

Marta Campo Dell'Orto (M)

Pathology Unit, Cà Foncello Regional Hospital, Treviso, Italy.

Luca M Saadeh (LM)

General Surgery Unit, University Hospital of Padova, Padova, Italy.

Francesco Ferrara (F)

Gastroenterology Unit (IV), Cà Foncello Regional Hospital, Treviso, Italy.

Stefano Benvenuti (S)

Gastroenterology Unit (IV), Cà Foncello Regional Hospital, Treviso, Italy.

Angelo P Dei Tos (AP)

Pathology Unit, Cà Foncello Regional Hospital, Treviso, Italy.

Nicolò Bassi (N)

Department of Surgery, Cà Foncello Regional Hospital, Treviso, Italy.

Andromachi Kotsafti (A)

Laboratory of Advanced Translational Research, Veneto Institute of Oncology (IOV-IRCCS), Padova, Italy.

Marco Scarpa (M)

General Surgery Unit, University Hospital of Padova, Padova, Italy, marcoscarpa73@yahoo.it.

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Classifications MeSH