Molecular and functional analysis of novel androgen receptor co-repressor in testicular cancer

为了验证AR转录活性降低与睾丸癌进展相关的假设，我们分析了新型AR共抑制因子ZNF288在睾丸癌细胞中的功能。结果表明，ZNF288能够与HDAC2和DNMT3B形成共抑制复合物，在TGCT模型细胞系中共抑制AR。此外，ZNF288在小鼠体内睾丸肿瘤发生实验中被证明是一个加速器。在精原细胞瘤模型细胞系TCam-2中，AR转录活性上调可抑制细胞生长。

To test the hypothesis that reduction in AR transcriptional activity is associated with progression of testicular cancer, we analyze the function of ZNF288, novel AR co-repressor in testicular cancer cells. The result demonstrated that ZNF288 was able to form a co-repressor complex with HDAC2 and DNMT3B, and co-represses AR in TGCT model cell lines. Moreover, ZNF288 was shown to be an accelerator in in vivo testicular tumorigenesis assays in mice. In TCam-2, seminoma model cell line, up-regulation of AR transcriptional activity repressed cell growth.