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EMMPRIN/CD147 up-regulates urokinase-type plasminogen activator: implications in oral tumor progression.
Lescaille G., Menashi S., Cavelier-Balloy B., Khayati F., Quemener C., Podgorniak M. Pierre, Naïmi B., Calvo F., Lebbe C., Mourah S.
BMC Cancer 12, 1 (2012) 115 - http://www.hal.inserm.fr/inserm-00694019
 (22443116) 
EMMPRIN/CD147 up-regulates urokinase-type plasminogen activator: implications in oral tumor progression.
Géraldine Lescaille1, Suzanne Menashi2, Bénédicte Cavelier-Balloy3, Farah Khayati1, Cathy Quemener1, Marie Podgorniak4, Benyoussef Naïmi2, Fabien Calvo1, Céleste Lebbe5, Samia Mourah () 1, 4
1 :  Hématologie -Immunologie -Cibles thérapeutiques
INSERM : U940 – Université Paris VII - Paris Diderot
France
2 :  CRRET - Croissance, Réparation et Régénération Tissulaires
EAC 7149 – Université Paris-Est Créteil Val-de-Marne (UPEC)
61 avenue du Général de Gaulle 94010 Créteil Cedex
France
3 :  Cabinet d'Anatomie Pathologique
Club de Dermatopathologie
35, avenue Mathurin Moreau, 75019 Paris
France
4 :  Laboratoire de Pharmacologie
Hôpital Saint-Louis – Assistance publique - Hôpitaux de Paris (AP-HP)
Paris F-75010
France
5 :  Département de Dermatologie
Hôpital Saint Louis
Paris F-75010, France
France
ABSTRACT: Backgrounds An elevated level of EMMPRIN in cancer tissues have been correlated with tumor invasion in numerous cancers including oral cavity and larynx. Although EMMPRIN's effect has been generally attributed to its MMP inducing activity, we have previously demonstrated in breast cancer model that EMMPRIN can also enhance invasion by upregulating uPA. In this study, the role of EMMPRIN in regulating uPA and invasion was investigated in oral squamous cell carcinoma (OSCC) progression. METHODS: Precancerous and invasive oral tumoral tissues were used as well as the corresponding cell lines, DOK and SCC-9 respectively. The paracrine regulation of uPA by EMMPRIN was investigated by treating culture cells with EMMPRIN-enriched membrane vesicles. UPA expression was analyzed by qPCR and immunostaining and the consequence on the invasion capacity was studied using modified Boyden chamber assay, in the presence or absence of EMMPRIN blocking antibody, the uPA inhibitor amiloride or the MMP inhibitor marimastat. RESULTS: OSCC tumors were shown to express more EMMPRIN and uPA compared to dysplastic lesions. The corresponding cell models, SCC-9 and DOK cells, displayed similar expression pattern. In both cell types EMMPRIN upregulated the expression of uPA as well as that of MMP-2 and MMP-9. EMMPRIN treatment led to a significant increase in cell invasion both in the invasive SCC-9 and in the less invasive dysplastic DOK cells, in an MMP and uPA dependent manner. CONCLUSIONS: Our results suggest that the upregulation of uPA contributes to EMMPRIN's effect in promoting oral tumor invasion.
Sciences du Vivant/Cancérologie
Anglais
1471-2407

Articles dans des revues avec comité de lecture
10.1186/1471-2407-12-115
BMC Cancer (BMC Cancer)
Publisher BioMed Central
ISSN 1471-2407 
internationale
23/03/2012
23/03/2012
12
1
115

EMMPRIN/CD147 – uPA – Oral squamous cell carcinoma – Invasion – Progression
Fondation pour la recherche médicale (FRM) (G. Lescaille), and PPF funding from Ministère de la Recherche and Conseil Régional Ile- De-France (confocal microscopy imaging).
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