Suppression of tumorigenicity in transformed cells after transfection with vinculin cDNA.
Suppression of tumorigenicity in transformed cells after transfection with vinculin cDNA.
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DOI：
10.1083/jcb.119.2.427
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发表时间：
1992-10
期刊：
影响因子：
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通讯作者：
Ben-Ze'ev A
中科院分区：
文献类型：
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作者：
Rodríguez Fernández JL;Geiger B;Salomon D;Sabanay I;Zöller M;Ben-Ze'ev A
将鸡纽蛋白基因导入两个内源性蛋白表达水平降低的肿瘤细胞系，可显著抑制其致瘤能力。SV-40转化的Balb/c 3T3细胞株(SVT2)的纽蛋白含量比亲本细胞少4倍，而大鼠腺癌细胞BSp73ASML中未检测到纽蛋白。将这些细胞中的纽蛋白恢复到3T3细胞中的水平，导致底物粘附性明显增加，在软琼脂中生长的能力下降，并在注射到同基因宿主或裸鼠体内后抑制它们发展成肿瘤的能力。这些结果表明，纽蛋白是细胞-基质和细胞-细胞黏附的细胞质成分，可能对转化的表型有重要的抑制作用。
Transfection of chicken vinculin cDNA into two tumor cell lines expressing diminished levels of the endogenous protein, brought about a drastic suppression of their tumorigenic ability. The SV-40-transformed Balb/c 3T3 line (SVT2) contains four times less vinculin than the parental 3T3 cells, and the rat adenocarcinoma BSp73ASML has no detectable vinculin. Restoration of vinculin in these cells, up to the levels found in 3T3 cells, resulted in an apparent increase in substrate adhesiveness, a decrease in the ability to grow in soft agar, and suppression of their capacity to develop tumors after injection into syngeneic hosts or nude mice. These results suggest that vinculin, a cytoplasmic component of cell-matrix and cell-cell adhesions, may have a major suppressive effect on the transformed phenotype.