Horikawa I, Yamada H, Kugoh H, Yuasa Y, Suzuki M, Oshimura M
Department of Molecular and Cell Genetics, School of Life Sciences, Faculty of Medicine, Tottori University, Yonago.
Jpn J Cancer Res. 1995 May;86(5):444-50. doi: 10.1111/j.1349-7006.1995.tb03077.x.
We previously reported that the introduction of a normal human chromosome 1 via microcell-mediated chromosome transfer suppressed the transformed phenotypes, including anchorage-independent growth, of Kirsten murine sarcoma virus-transformed NIH3T3 (DT) cells. Soft-agar clones derived from DT-#1 cells (DT cells with an intact transferred human chromosome 1) exclusively failed to retain an intact form of this chromosome. Thus, a gene(s) with a suppressive activity on this chromosome had probably been lost. We therefore attempted to identify a commonly deleted region on human chromosome 1 in these soft-agar clones. Although eight of the 9 soft-agar clones examined still contained regions on this chromosome, to a greater or lesser degree, four loci on 1q21 and 1q23-q24 were commonly lost in all of them. Furthermore, the soft-agar clones had growth properties similar to those of DT cells. Thus, chromosome and DNA analyses suggested that human 1q21 and/or 1q23-q24 carries a transformation suppressor gene(s) which controls the transformed phenotypes of DT cells.
我们先前报道过，通过微细胞介导的染色体转移引入正常人类1号染色体可抑制 Kirsten 小鼠肉瘤病毒转化的 NIH3T3（DT）细胞的转化表型，包括不依赖贴壁生长。源自DT-#1细胞（带有完整转入人类1号染色体的DT细胞）的软琼脂克隆唯独未能保留该染色体的完整形式。因此，该染色体上具有抑制活性的一个或多个基因可能已丢失。我们因此试图在这些软琼脂克隆中确定人类1号染色体上的一个常见缺失区域。尽管所检测的9个软琼脂克隆中有8个在不同程度上仍含有该染色体上的区域，但1q21和1q23-q24上的4个位点在所有克隆中均普遍缺失。此外，软琼脂克隆具有与DT细胞相似的生长特性。因此，染色体和DNA分析表明，人类1q21和/或1q23-q24携带一个控制DT细胞转化表型的转化抑制基因。
