Hatakeyama S, Suzuki A, Yoshizumi N, Sato M, Nishiya I
Department of Oral Pathology, School of Dentistry, Iwate Medical University, Morioka, Japan.
Cell Biol Int Rep. 1991 Jan;15(1):55-65. doi: 10.1016/0309-1651(91)90082-t.
Dexamethasone (1 microM) decreased the distribution of cells in S phase (about 75%) and increased that of G1 cells (1.1-fold) in the DNA histogram of human submandibular salivary gland adenocarcinoma cells (HSG) reversibly. In synchronized cells at G1 phase, glucocorticoid delayed the initiation of DNA synthesis by about 3-4 h. The conditioned medium (50%) or exogenous human epidermal growth factor (EGF, 10 ng/ml) significantly nullified these effects by glucocorticoids. These results suggested that glucocorticoids arrested the cells at G1 phase, which implied the inhibition of production of some progressive factor, probably EGF, in the cell cycle of HSG.
地塞米松（1微摩尔）可逆地降低了人下颌下唾液腺腺癌细胞（HSG）DNA直方图中处于S期的细胞分布（约75%），并使G1期细胞分布增加（1.1倍）。在G1期同步化的细胞中，糖皮质激素将DNA合成的起始延迟了约3 - 4小时。条件培养基（50%）或外源性人表皮生长因子（EGF，10纳克/毫升）显著消除了糖皮质激素的这些作用。这些结果表明，糖皮质激素使细胞停滞在G1期，这意味着在HSG细胞周期中抑制了某种促进因子的产生，可能是EGF。
