Implication of chromosome 11 in the suppression of neoplastic expression in human cell hybrids.
Implication of chromosome 11 in the suppression of neoplastic expression in human cell hybrids.
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发表时间：
1986-12
期刊：
影响因子：
11.2
通讯作者：
E. Srivatsan;W. Benedict;E. Stanbridge
中科院分区：
文献类型：
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作者：
E. Srivatsan;W. Benedict;E. Stanbridge
种内人类HeLa X成纤维细胞杂交细胞群的细胞遗传学分析提供了初步证据，证明了11号和14号染色体单拷贝丢失与致瘤性再表达的相关性。在这项研究中，成对的组合nontumorigenic和致瘤性分离HeLa X成纤维细胞杂交细胞从两个独立的融合事件进行了检查是否存在正常的染色体11和14。在人类杂交细胞系中，染色体的亲本来源可以根据限制性片段长度多态性来区分。基因c-Ha-ras，胰岛素，载脂蛋白A-1的染色体11和一个多态性位点AW 101染色体14上被用作Southern杂交探针。从父母的成纤维细胞和HeLa细胞系和它们的nontumorigenic和tumorigenic杂交的DNA分析表明，在4个致瘤分离和HeLa染色体11在第五个杂交细胞系的成纤维细胞染色体11的损失。有趣的是，后一种分离子也丢失了成纤维细胞来源的14号染色体的拷贝。在任何其他杂交细胞群中，正常14号染色体拷贝丢失与致瘤性重新表达之间没有明显的相关性。我们从这些观察中得出的结论是，定位于正常11号染色体的基因可能参与了这些人类杂交细胞中致瘤表达的控制。
Cytogenetic analyses of intraspecies human HeLa X fibroblast hybrid cell populations have provided tentative evidence for the correlation of loss of a single copy of chromosomes 11 and 14 with reexpression of tumorigenicity. In this study paired combinations of nontumorigenic and tumorigenic segregant HeLa X fibroblast hybrid cells from two independent fusion events were examined for the presence or absence of normal chromosomes 11 and 14. In human hybrid cell lines the parental origin of chromosomes can be distinguished on the basis of restriction fragment length polymorphisms. Genes for c-Ha-ras, insulin, and apolipoprotein A-1 on chromosome 11 and a polymorphic locus AW101 on chromosome 14 were used as Southern hybridization probes. Analysis of DNA from the parental fibroblast and HeLa cell lines and their nontumorigenic and tumorigenic hybrids showed the loss of a fibroblast chromosome 11 in four of the tumorigenic segregants and a HeLa chromosome 11 in a fifth hybrid cell line. This latter segregant has, interestingly, also lost a copy of chromosome 14 of fibroblast origin. There was no obvious correlation of loss of a copy of normal chromosome 14 and reexpression of tumorigenicity in any of the other hybrid cell populations. Our conclusion from these observations is that gene(s) that map to normal chromosome 11 might be involved in control of tumorigenic expression in these human hybrid cells.