论文部分内容阅读
人前列腺特异抗原(PSA)基因的表达受雄激素的调节。其雄激素应答元件(ARE)位于—170附近。为确定雄激素对该基因的诱导作用是否受ARE上游序列的影响,把PSA启动子区的不同长度的天然的和变异的DNA片段分别与报告基因CAT相连,构建成了不同的PBLCAT3—PSA表达质粒,然后转染人前列腺肿瘤细胞PC—3。结果表明ARE上游RF15(-340—-326)序列的缺失和变异可显著降低雄激素对PSA基因的诱导作用。RF15序列可与LNcap和PC—3细胞中的某些调节蛋白结合。这些调节蛋白可能通过与雄激素受体的相互作用影响雄激素对PSA基因的诱导作用。
The expression of human prostate-specific antigen (PSA) genes is regulated by androgens. Its androgen response element (ARE) is located near -170. To determine whether the induction of androgen by this gene is affected by the upstream sequence of ARE, different lengths of natural and variant DNA fragments in the PSA promoter region were ligated with the reporter gene CAT to construct different PBLCAT3-PSA expression Plasmids were then transfected into human prostate tumor cells PC-3. The results showed that the deletion and mutation of RF15 (-340 - 326) upstream of ARE significantly decreased the induction of PSA by PSA. The RF15 sequence binds to some of the regulatory proteins in LNcap and PC-3 cells. These regulatory proteins may affect the androgen induction of PSA gene through the interaction with androgen receptor.