Institute of Dentistry, University of Helsinki, and Department of Oral and Maxillofacial Diseases, Helsinki University Hospital, Helsinki, Finland.
Cancer Invest. 2012 Oct;30(8):583-92. doi: 10.3109/07357907.2012.716467. Epub 2012 Aug 21.
Enhanced proteolysis and altered tight junction (TJ) proteins associate with carcinoma invasion. We hypothesized that trypsin-2, a tumor-associated serine proteinase, induces tongue carcinoma invasion by activating pro-membrane type-1 matrix metalloproteinase (MT1-MMP) and disturbing the TJs. The effects of invasion were analyzed using trypsin-2 over-expressing human tongue squamous cell carcinoma cells (Try2-HSC-3) in vitro and in vivo. The invasion of Try2-HSC-3 cells was increased in mouse xenografts and human organotypic model. Trypsin-2 activated proMT1-MMP, as well as altered the expression of TJ protein claudin-7. In conclusion, trypsin-2 over-expression enhanced tongue carcinoma cell invasion by various genetic and proteolytic mechanisms.
增强的蛋白水解和紧密连接（TJ）蛋白的改变与癌浸润有关。我们假设胰蛋白酶-2（一种与肿瘤相关的丝氨酸蛋白酶）通过激活前膜型 1 基质金属蛋白酶（MT1-MMP）和扰乱 TJ 来诱导舌癌浸润。通过体外和体内实验，分析了侵袭的效果，在小鼠异种移植和人器官型模型中，Try2-HSC-3 细胞的侵袭增加。胰蛋白酶-2激活了 proMT1-MMP，同时改变了 TJ 蛋白 Claudin-7 的表达。总之，胰蛋白酶-2 的过度表达通过各种遗传和蛋白水解机制增强了舌癌细胞的侵袭。
