Identification of a single chromosome in the normal human genome essential for suppression of hamster cell transformation.
Identification of a single chromosome in the normal human genome essential for suppression of hamster cell transformation.
复制标题
鉴定正常人类基因组中对于抑制仓鼠细胞转化至关重要的单个染色体。
DOI：
10.1073/pnas.82.2.570
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发表时间：
1985
影响因子：
11.1
通讯作者：
Bouck,N
中科院分区：
文献类型：
--
作者：
Stoler,A;Bouck,N
将正常的人成纤维细胞融合到致癌物质转化的幼鼠肾细胞（BHK）中，发现能够抑制仓鼠细胞的锚定非依赖性转化表型。这种抑制不是由于种间不亲和性，因为如果人类或BHK亲本最初被显性病毒基因组转化，则转化可以有效地表达在杂交种中。当被抑制的杂交体生长时，人类染色体的丢失伴随着转化的重新表达。核型分析表明，在所有被抑制的杂交种中，只保留了人类染色体1，而在所有重新表达转化的杂交种中，染色体1缺失。1号染色体存在或不存在的细胞学证据是通过磷酸葡萄糖糖化酶1的人同工酶的电泳鉴定证实的。从两个抑制的杂交种中分离出了重新表达转化的克隆，在这两种情况下，抑制的丧失都伴随着人类1号染色体的丧失。因此，在这些跨物种杂交中维持抑制似乎需要正常人类1号染色体的持续存在。这些发现提出了一种可能性，即人类1号染色体经常参与人类肿瘤中潜在的失活畸变，这可能反映了该染色体在人类恶性肿瘤中的抑制作用。
Normal human fibroblasts were fused to carcinogen-transformed baby hamster kidney (BHK) cells and found to be able to suppress the anchorage-independent transformed phenotype of the hamster cells. This suppression was not due to interspecies incompatibility, for transformation could be effectively expressed in hybrids if either the human or the BHK parent had initially been transformed by a dominantly acting viral genome. Upon growth of suppressed hybrids, loss of human chromosomes was accompanied by the re-expression of transformation. Karyotype analysis indicated that only human chromosome 1 was retained in all hybrids that were suppressed and was lost in all hybrids in which transformation was re-expressed. Cytological evidence for the presence or absence of chromosome 1 was confirmed by electrophoretic identification of the human isozyme for phosphoglucomutase 1. Clones re-expressing transformation were isolated from two suppressed hybrids and in both cases loss of suppression was accompanied by the loss of human chromosome 1. Thus, the maintenance of suppression in these cross-species hybrids appears to require the continued presence of normal human chromosome 1. These findings raise the possibility that the frequent involvement of human chromosome 1 in potentially inactivating aberrations in human tumors may reflect a suppressor role for this chromosome in human malignancy.