Lascombe I, Sallot M, Vuillermoz C, Weisz A, Adessi G L, Jouvenot M
I.E.T.G., Bâtiment INSERM, Besançon, France.
Mol Cell Endocrinol. 1998 Apr 30;139(1-2):153-60. doi: 10.1016/s0303-7207(98)00064-1.
Our previous results have suggested a repression of E2 (17beta-estradiol) effect on the c-fos gene of cultured guinea-pig endometrial cells. To investigate this repression, the expression of three human c-fos gene recombinants, pFC1-BL (-2250/+41), pFC2-BL (-1400/+41) and pFC2E (-1300/-1050 and -230/+41), known to be E2-responsive in Hela cells, was studied in stromal (SC) and glandular epithelial cells (GEC). In both cellular types, pFC1-BL was not induced by E2, even in the presence of growth factors or co-transfected estrogen receptor. The pattern of pFC2-BL and pFC2E expression was strikingly different and depended on the cellular type: pFC2-BL and pFC2E induction was restricted to the glandular epithelial cells and did not occur in the SCs. We argue for a repression of E2 action which is dependent on the estrogen-responsive cis-acting element (ERE) environment and also cell type-specific involving DNA/protein and/or protein/protein interactions with cellular type-specific factors.
我们之前的研究结果表明，17β-雌二醇（E2）对培养的豚鼠子宫内膜细胞的c-fos基因存在抑制作用。为了探究这种抑制作用，我们研究了三种已知在Hela细胞中对E2有反应的人c-fos基因重组体pFC1-BL（-2250/+41）、pFC2-BL（-1400/+41）和pFC2E（-1300/-1050和-230/+41）在基质细胞（SC）和腺上皮细胞（GEC）中的表达情况。在这两种细胞类型中，即使存在生长因子或共转染雌激素受体，E2也不会诱导pFC1-BL的表达。pFC2-BL和pFC2E的表达模式显著不同，且取决于细胞类型：pFC2-BL和pFC2E的诱导仅限于腺上皮细胞，在基质细胞中不会发生。我们认为E2作用的抑制取决于雌激素反应性顺式作用元件（ERE）环境，并且还涉及细胞类型特异性的DNA/蛋白质和/或蛋白质/蛋白质与细胞类型特异性因子的相互作用。
