Ara T, Deyama Y, Yoshimura Y, Higashino F, Shindoh M, Matsumoto A, Fukuda H
First Department of Oral Surgery, School of Dentistry, Hokkaido University, Kita 13 Nishi 7, kita-ku, 060-8586, Sapporo, Japan.
Cancer Lett. 2000 Sep 1;157(2):115-21. doi: 10.1016/s0304-3835(00)00494-8.
To elucidate the role of E-cadherin in matrix metalloproteinases (MMPs) expression, we transfected to squamous carcinoma cells with E-cadherin cDNA. HN5 cells and mock-transfected HN5-neo cells expressed proMMP-2 and active MMP-2. E-cadherin-transfected HN5-EC cells produced comparable proMMP-2 but low active MMP-2; and membrane type 1-MMP (MT1-MMP) mRNA declined. Phosphorylated ERK, a marker of mitogen-activated protein (MAP) kinase cascade, also declined in HN5-EC cells. The addition of anti-E-cadherin antibody resulted in the disappearance of these alterations in HN5-EC cells. These results suggest that E-cadherin suppresses MAP kinase cascade and down-regulates MT1-MMP.
为阐明E-钙黏蛋白在基质金属蛋白酶（MMPs）表达中的作用，我们用E-钙黏蛋白cDNA转染鳞状癌细胞。HN5细胞和mock转染的HN5-neo细胞表达前MMP-2和活性MMP-2。E-钙黏蛋白转染的HN5-EC细胞产生相当的前MMP-2，但活性MMP-2水平较低；膜型1-MMP（MT1-MMP）mRNA水平下降。有丝分裂原活化蛋白（MAP）激酶级联反应的标志物磷酸化ERK在HN5-EC细胞中也下降。添加抗E-钙黏蛋白抗体导致HN5-EC细胞中的这些改变消失。这些结果表明，E-钙黏蛋白抑制MAP激酶级联反应并下调MT1-MMP。
