Mareel M, Bracke M, Van Roy F
Department of Radiotherapy, Nuclear Medicine and Experimental Cancerology, University Hospital, Ghent, Belgium.
Cancer Detect Prev. 1995;19(5):451-64.
Invasion is the hallmark of tumor malignancy. We situate invasion within microecosystems comprising neoplastic cells as well as host cells. Modulation of invasion within such systems is ascribed to balances between promoter and suppressor pathways. The E-cadherin/alpha-, beta-, gamma-catenin complex has an invasion-suppressor function as evidenced by transfections either with sense cDNA encoding these molecules or with antisense cDNA inhibiting their expression. Loss of heterozygosity at the E-Cadherin (uvo) locus has been reported, but mutations in the E-cadherin gene seem to be rare. Downregulation of E-cadherin occurred at the level of transcription or of mRNA stability. Ex vivo cultures from invasive tumors or metastases produced cells that were homogeneously E-cadherin-positive and noninvasive in vitro. These observations have led to the idea that factors in the host downmodulate the E-cadherin complex and promote invasion most probably in a transient way.
侵袭是肿瘤恶性的标志。我们将侵袭置于由肿瘤细胞以及宿主细胞组成的微生态系统中。在这样的系统中，侵袭的调节归因于促进途径和抑制途径之间的平衡。E-钙黏蛋白/α、β、γ-连环蛋白复合体具有侵袭抑制功能，这可通过转染编码这些分子的正义cDNA或抑制其表达的反义cDNA来证明。据报道，E-钙黏蛋白（uvo）基因座存在杂合性缺失，但E-钙黏蛋白基因突变似乎很少见。E-钙黏蛋白的下调发生在转录水平或mRNA稳定性水平。来自侵袭性肿瘤或转移灶的体外培养产生的细胞在体外是均匀E-钙黏蛋白阳性且无侵袭性的。这些观察结果引发了这样一种观点，即宿主中的因素最有可能以一种短暂的方式下调E-钙黏蛋白复合体并促进侵袭。
