Van Meir E G, Polverini P J, Chazin V R, Su Huang H J, de Tribolet N, Cavenee W K
Ludwig Institute for Cancer Research, University of California at San Diego, La Jolla 92093-0660.
Nat Genet. 1994 Oct;8(2):171-6. doi: 10.1038/ng1094-171.
The earliest genetic alteration in human astrocytoma progression is mutation of the p53 tumour suppressor gene, while one of the earliest phenotypic changes is the stimulation of neovascularization. Here, we tested the role of p53 in the angiogenic process by introducing a tetracycline-regulated wild type p53 gene into null glioblastoma cells. The parental cells expressed strong angiogenic activity while upon induction of wild type, but not mutant, p53 expression, the cells secreted a factor able to neutralize the angiogenicity of the factors produced by the parental cells as well as of basic fibroblast growth factor.
人类星形细胞瘤进展过程中最早出现的基因改变是p53肿瘤抑制基因的突变，而最早出现的表型变化之一是新血管形成的刺激。在此，我们通过将四环素调控的野生型p53基因导入p53基因缺失的胶质母细胞瘤细胞，来测试p53在血管生成过程中的作用。亲代细胞表现出很强的血管生成活性，而在诱导野生型（而非突变型）p53表达后，这些细胞分泌出一种因子，该因子能够中和亲代细胞以及碱性成纤维细胞生长因子所产生的因子的血管生成活性。
