Koi M, Afshari C A, Annab L A, Barrett J C
Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709.
Proc Natl Acad Sci U S A. 1989 Nov;86(22):8773-7. doi: 10.1073/pnas.86.22.8773.
Tumor-suppressor genes control the neoplastic phenotype of tumor cells, but the function of these genes in normal cells is unknown. In this report we show that the loss of a tumor-suppressor gene function releases negative controls on the growth of cells in agar. This conclusion is based on observations of cell hybrids and studies of cell variants that have retained or lost a tumor-suppressor gene function. Nontumorigenic cell hybrids between normal Syrian hamster embryo cells and a benzo[a]pyrene-transformed tumor-cell line (BP6T) continued to secrete autocrine and/or paracrine growth factors produced by the tumor cells but failed to respond to these factors by growing in agar. Normal diploid cells also failed to grow in agar in response to the growth factors produced by the tumor cells. Clonal variants of nontumorigenic, immortal Syrian hamster cell lines were isolated that either retained (termed supB+) or had lost (termed supB-) the ability to suppress tumorigenicity of BP6T tumor cells after cell hybridization. Neither supB+ nor supB- variants grew in agar under conditions that allowed efficient growth of the tumor cells. However, supB- cells were reversibly induced to grow in agar with high colony-forming efficiencies in the presence of tumor cell-conditioned medium or by supplementation of the medium with a combination of growth factors. Under the same conditions, the supB+ cells failed to grow in agar. This enhanced growth-factor responsiveness in agar was used to select for supB- variants existing at a low frequency in the supB+ population. These two phenotypes, loss of tumor-suppressor function and enhanced growth-factor responsiveness in agar, were seen to cosegregate. These results indicate the tumor-suppressor gene function in these cells negatively regulates the growth response of cells in agar to mitogenic stimuli. This growth regulation may depend on cell shape or adhesion because supB+ and supB- cells grown attached to plastic responded similarly to growth factors.
肿瘤抑制基因控制肿瘤细胞的肿瘤表型,但这些基因在正常细胞中的功能尚不清楚。在本报告中,我们表明肿瘤抑制基因功能的丧失会解除对琼脂中细胞生长的负调控。这一结论基于对细胞杂交体的观察以及对保留或丧失肿瘤抑制基因功能的细胞变体的研究。正常叙利亚仓鼠胚胎细胞与苯并[a]芘转化的肿瘤细胞系(BP6T)之间的非致瘤性细胞杂交体继续分泌肿瘤细胞产生的自分泌和/或旁分泌生长因子,但在琼脂中生长时未能对这些因子作出反应。正常二倍体细胞对肿瘤细胞产生的生长因子也不能在琼脂中生长。分离出非致瘤性永生叙利亚仓鼠细胞系的克隆变体,这些变体在细胞杂交后要么保留(称为supB +)要么丧失(称为supB -)抑制BP6T肿瘤细胞致瘤性的能力。在允许肿瘤细胞高效生长的条件下,supB +和supB -变体在琼脂中均不生长。然而,在肿瘤细胞条件培养基存在下或通过向培养基中添加生长因子组合,supB -细胞可被可逆地诱导在琼脂中生长,且集落形成效率高。在相同条件下,supB +细胞在琼脂中不能生长。利用琼脂中这种增强的生长因子反应性来选择在supB +群体中以低频率存在的supB -变体。这两种表型,即肿瘤抑制功能的丧失和琼脂中生长因子反应性的增强,被发现是共分离的。这些结果表明,这些细胞中的肿瘤抑制基因功能对琼脂中细胞对有丝分裂刺激的生长反应起负调控作用。这种生长调节可能取决于细胞形状或黏附,因为附着在塑料上生长的supB +和supB -细胞对生长因子的反应相似。