Induction of alpha2-antiplasmin inhibits E-cadherin processing mediated by the plasminogen activator/plasmin system, leading to suppression of progression of oral squamous cell carcinoma via upregulation of cell-cell adhesion

The plasminogen activator/plasmin system is one of the main protease systems involved in tumor cell invasion and metastasis. Our previous study has shown that plasmin degrades E-cadherin and promotes cell dissemination by downregulation of E-cadherin-mediated cell-cell adhesion in oral squamous cell...

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Published inOncology reports Vol. 17; no. 2; pp. 417 - 423
Main Authors Hayashido, Yasutaka, Hamana, Tomoaki, Ishida, Yasutaka, Shintani, Tomoaki, Koizumi, Koh-Ichi, Okamoto, Tetsuji
Format Journal Article
LanguageEnglish
Published Greece 01.02.2007
Subjects
alpha-2-Antiplasmin - metabolism
Animals
Cadherins - metabolism
Carcinoma, Squamous Cell - metabolism
Carcinoma, Squamous Cell - pathology
Cell Adhesion
Collagen - metabolism
Disease Progression
Fibrinolysin - metabolism
Gene Expression Regulation, Neoplastic
Humans
Male
Mice
Mice, Inbred BALB C
Mice, Nude
Mouth Neoplasms - metabolism
Plasminogen Activators - metabolism
Up-Regulation
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Summary:The plasminogen activator/plasmin system is one of the main protease systems involved in tumor cell invasion and metastasis. Our previous study has shown that plasmin degrades E-cadherin and promotes cell dissemination by downregulation of E-cadherin-mediated cell-cell adhesion in oral squamous cell carcinoma (SCC) cells. To examine the effect of downregulation of the plasminogen activator/plasmin system by alpha2-antiplasmin (alpha2-AP) on cell-cell adhesion mediated by E-cadherin in oral SCC cells, the oral SCC cell line SCCKN was stably transfected with alpha2-AP cDNA. Induction of alpha2-AP expression led to the inhibition of the proteolysis of E-cadherin by plasminogen activator/plasmin in SCC cells, resulting in the enhancement of the cell aggregation and the suppression of the cell motility. Moreover, alpha2-AP also reduced the ability of SCC cells to invade type I collagen gel, and suppressed tumorigenicity in vivo. These results suggested that downregulation of the plasminogen activator/ plasmin system by alpha2-AP might be a potent therapeutic approach to prevent the progression of oral SCC.
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ISSN:1021-335X
1791-2431