猴病毒40小t抗原增强v-src转化活性。

W B Wang, T M Kao, C Yang
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摘要

已知猿猴病毒40 (SV40)小t (t)抗原能够诱导细胞增殖并增强SV40大t抗原的转化活性。这里我们报道t也可以增强v-src癌基因的转化活性。将t转染到v-src转化的NIH3T3细胞中,表达t的稳定克隆比亲本或载体转染的细胞生长更快,生长密度更高。此外,这些表达t的细胞也表现出更好的镀膜效率,并且在软琼脂中比亲本或载体转染的细胞更有效地生长。更重要的是,表达t的细胞表现出高度聚集和容易脱离培养皿的倾向,而亲代或载体转染的细胞从未表现出这种表型。最后的观察结果表明,t可能会影响v-src转化的NIH3T3细胞中粘附分子的表达。综上所述,我们认为t可以增强v-src的转化活性,改变v-src转化的NIH3T3细胞的转化形态。
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Enhancement of v-src transforming activity by simian virus 40 small t antigen.

The simian virus 40 (SV40) small t (t) antigen is known to be able to induce cell proliferation and to enhance the transforming activity of SV40 large T antigen. Here we report that t could also enhance the transforming activity of v-src oncogene. When t was transfected into the v-src-transformed NIH3T3 cells, the t-expressing stable clones grew faster and grew to higher density than did the parental or vector-transfected cells. Furthermore, these t-expressing cells also showed better plating efficiency and grew more efficiently in soft agar than did the parental or vector-transfected cells. More importantly, the t-expressing cells displayed high tendency to aggregate and detached easily from the dishes, while the parental or vector-transfected cells never exhibited such phenotype. This last observation suggests that t may affect the expression of adhesion molecules in the v-src-transformed NIH3T3 cells. Taken together, we concluded that t could enhance the transforming activity of v-src and alter the transformed morphology of v-src-transformed NIH3T3 cells.

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