Horvath G, Leser G, Delle U
Division of Gynaecological Oncology, Sahlgrenska University Hospital, Gothenburg, Sweden.
In Vivo. 1996 Jan-Feb;10(1):29-32.
The influence of different estradiol concentrations on the expression of the p53 suppressor gene and on cell kinetics was examined by semiquantitative analysis of protein and bromodeoxyuridine labelling in a human endometrial adenocarcinoma grown in nude mice. We found that increasing the circulating estradiol increases (p = 0.001), and decreasing the hormone value decreases (p = 0.001) the expression of p53 in this tumor. The number of cells in the G1/G0 phase of the cell cycle was significantly higher (p = 0.03), and the number of cells in the G2/M phase was significantly lower (p = 0.01) in tumors grown in estradiol-treated mice than in tumors obtained from the nontreated group. Changes in p53 expression may possibly be explained by either altered transcription activity of the gene or increased half-life of the protein. Our results suggest an important role of estradiol in the progression of estrogen receptor (ER) positive human endometrial adenocarcinomas.
通过对裸鼠体内生长的人子宫内膜腺癌中蛋白质和溴脱氧尿苷标记进行半定量分析，研究了不同雌二醇浓度对p53抑癌基因表达及细胞动力学的影响。我们发现，循环雌二醇水平升高会使该肿瘤中p53的表达增加（p = 0.001），而激素水平降低则会使其表达减少（p = 0.001）。与未处理组的肿瘤相比，用雌二醇处理的小鼠所生长肿瘤的细胞周期G1/G0期细胞数量显著增加（p = 0.03），G2/M期细胞数量显著减少（p = 0.01）。p53表达的变化可能是由于基因转录活性改变或蛋白质半衰期延长所致。我们的结果表明，雌二醇在雌激素受体（ER）阳性的人子宫内膜腺癌进展中起重要作用。
