Journal
INTERNATIONAL JOURNAL OF CANCER
Volume 128, Issue 2, Pages 283-293Publisher
WILEY
DOI: 10.1002/ijc.25326
Keywords
plasminogen activator; angiogenesis; lymphangiogenesis; K14-HPV16
Categories
Funding
- European Union [201279]
- Fonds de la Recherche Scientifique Medicale
- Fonds National de la Recherche Scientifique (F.N.R.S., Belgium)
- Fondation Contre le Cancer
- Fonds Speciaux de la Recherche (University of Liege)
- Centre Anticancereux Pres l'Universite de Liege
- Fonds Leon Fredericq (University of Liege)
- Region Wallonne
- Interuniversity Attraction Poles Programme Belgian Science Policy (Brussels, Belgium)
- Televie-FNRS
- NIH/NCI
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Angiogenesis, extracellular matrix remodeling and cell migration are associated with cancer progression and involve at least, the plasminogen activating system and its main physiological inhibitor, the plasminogen activator inhibitor-1 (PAI-1). Considering the recognized importance of PAI-1 in the regulation of tumor angiogenesis and invasion in murine models of skin tumor transplantation, we explored the functional significance of PAI-1 during early stages of neoplastic progression in the transgenic mouse model of multistage epithelial carcinogenesis (K14-HPV16 mice). We have studied the effect of genetic deletion of PAI-1 on inflammation, angiogenesis, lymphangiogenesis and tumor progression. In this model, PAI-1 deficiency neither impaired keratinocyte hyperproliferation or tumor development nor affected the infiltration of inflammatory cells and development of angiogenic or lymphangiogenic vasculature. We are reporting evidence for concomitant lymphangiogenic and angiogenic switches independent to PAI-1 status. Taken together, these data indicate that PAI-1 is not rate limiting for neoplastic progression and vascularization during premalignant progression, or that there is a functional redundancy between PAI-1 and other tumor regulators, masking the effect of PAI-1 deficiency in this long-term model of multistage epithelial carcinogenesis.
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