Miłoszewska J, Szaniawska B, Trembacz H, Gos M, Przybyszewska M, Swoboda P, Małecki M, Janik P
Cell Biology Department, Cancer Center, W.K. Roentgen 5, 02-781 Warsaw, Poland.
Cell Prolif. 2006 Jun;39(3):195-203. doi: 10.1111/j.1365-2184.2006.00382.x.
The density-dependent growth inhibition of non-transformed cells may be associated with inefficient transduction of the proliferative signal from cell adhesion molecules. To verify this concept, the C3H10T1/2 fibroblasts were stably transfected with the gene coding for the fibronectin fragment III/10 (FNIII/10). This resulted in differences in gene's expression between original C3H10T1/2 cells and their FNIII/10 transfectants. No significant differences in growth properties were observed in the original or in the transfected cells. C3H10T1/2 cells and their transfectants, when co-cultured, displayed more cells at confluence than the cells cultured alone. Moreover, co-cultured C3H10T1/2 cells and their transfectants showed elevated levels of phospho-ERK1/2 compared to homogenous cultures. Results obtained indicate that cellular homogeneity is responsible for density-dependent growth inhibition.
非转化细胞的密度依赖性生长抑制可能与细胞黏附分子增殖信号的转导效率低下有关。为了验证这一概念,将编码纤连蛋白片段III/10(FNIII/10)的基因稳定转染到C3H10T1/2成纤维细胞中。这导致原始C3H10T1/2细胞与其FNIII/10转染子之间基因表达存在差异。在原始细胞或转染细胞中未观察到生长特性的显著差异。C3H10T1/2细胞及其转染子在共培养时,汇合时的细胞比单独培养的细胞更多。此外,与同质培养相比,共培养的C3H10T1/2细胞及其转染子显示出磷酸化ERK1/2水平升高。所得结果表明细胞同质性是密度依赖性生长抑制的原因。