Unimpeded skin carcinogenesis in K14-HPV16 transgenic mice deficient for plasminogen activator inhibitor

Anne Masset, Catherine Maillard, Nor Eddine Sounni, Nathalie Jacobs, Françoise Bruyére, Philippe Delvenne, Marlene Tacke, Thomas Reinheckel, Jean Michel Foidart, Lisa Coussens, Agnès Noaël

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)283-293
Number of pages11
JournalInternational Journal of Cancer
Volume128
Issue number2
DOIs
StatePublished - Jan 15 2011
Externally publishedYes

Fingerprint

Plasminogen Inactivators
Plasminogen Activator Inhibitor 1
Transgenic Mice
Carcinogenesis
Skin
Neoplasms
Lymphangiogenesis
Skin Transplantation
Plasminogen
Keratinocytes
Cell Movement
Extracellular Matrix
Inflammation

Keywords

  • angiogenesis
  • K14-HPV16
  • lymphangiogenesis
  • plasminogen activator

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Masset, A., Maillard, C., Sounni, N. E., Jacobs, N., Bruyére, F., Delvenne, P., ... Noaël, A. (2011). Unimpeded skin carcinogenesis in K14-HPV16 transgenic mice deficient for plasminogen activator inhibitor. International Journal of Cancer, 128(2), 283-293. https://doi.org/10.1002/ijc.25326

Unimpeded skin carcinogenesis in K14-HPV16 transgenic mice deficient for plasminogen activator inhibitor. / Masset, Anne; Maillard, Catherine; Sounni, Nor Eddine; Jacobs, Nathalie; Bruyére, Françoise; Delvenne, Philippe; Tacke, Marlene; Reinheckel, Thomas; Foidart, Jean Michel; Coussens, Lisa; Noaël, Agnès.

In: International Journal of Cancer, Vol. 128, No. 2, 15.01.2011, p. 283-293.

Research output: Contribution to journalArticle

Masset, A, Maillard, C, Sounni, NE, Jacobs, N, Bruyére, F, Delvenne, P, Tacke, M, Reinheckel, T, Foidart, JM, Coussens, L & Noaël, A 2011, 'Unimpeded skin carcinogenesis in K14-HPV16 transgenic mice deficient for plasminogen activator inhibitor', International Journal of Cancer, vol. 128, no. 2, pp. 283-293. https://doi.org/10.1002/ijc.25326
Masset, Anne ; Maillard, Catherine ; Sounni, Nor Eddine ; Jacobs, Nathalie ; Bruyére, Françoise ; Delvenne, Philippe ; Tacke, Marlene ; Reinheckel, Thomas ; Foidart, Jean Michel ; Coussens, Lisa ; Noaël, Agnès. / Unimpeded skin carcinogenesis in K14-HPV16 transgenic mice deficient for plasminogen activator inhibitor. In: International Journal of Cancer. 2011 ; Vol. 128, No. 2. pp. 283-293.
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