Armelin M C, Armelin H A
Proc Natl Acad Sci U S A. 1978 Jun;75(6):2805-9. doi: 10.1073/pnas.75.6.2805.
Hydrocortisone at physiological concentrations reversibly inhibits DNA synthesis in ST1 cells (a line of mouse fibroblasts possessing 40 chromosomes and derived from Swiss 3T3 cells). This inhibitory activity is a property of glucocorticoids, but the beta-OH of C-11 of glucocorticoids is not essential for the inhibition. The steroid hormone restores to ST1 cells dependency on serum, density, and anchorage for growth. When injected into nude mice, ST1 cells generated malignant invasive fibrosarcoma. Injections of dexamethasone into tumor-bearing animals blocked tumor growth. The steroid hormone seems to induce a reversible transition between a transformed and a "normal" phenotype. ST1 cells treated or untreated with hydrocotisone are not responsive to fibroblast growth factor, epidermal growth factor, or prostaglandin F2alpha whereas they are responsive to a factor that is a contaminant in bovine serum albumin.
生理浓度的氢化可的松可可逆地抑制ST1细胞（源自瑞士3T3细胞、拥有40条染色体的小鼠成纤维细胞系）中的DNA合成。这种抑制活性是糖皮质激素的特性，但糖皮质激素C-11位的β-OH对于抑制并非必不可少。该甾体激素可使ST1细胞恢复对血清、密度和贴壁生长的依赖性。将ST1细胞注射到裸鼠体内时，会产生恶性侵袭性纤维肉瘤。向荷瘤动物注射地塞米松可阻断肿瘤生长。该甾体激素似乎可诱导在转化型和“正常”表型之间的可逆转变。无论是否用氢化可的松处理，ST1细胞对成纤维细胞生长因子、表皮生长因子或前列腺素F2α均无反应，而它们对牛血清白蛋白中的一种污染物因子有反应。
