The oncogenic transcription factor ERG represses the transcription of the tumour suppressor gene PTEN in prostate cancer cells
The oncogenic transcription factor ERG represses the transcription of the tumour suppressor gene PTEN in prostate cancer cells
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DOI：
10.3892/ol.2017.6841
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发表时间：
2017-11-01
期刊：
影响因子：
2.9
通讯作者：
Ladomery, Michael R.
中科院分区：
文献类型：
--
作者：
Adamo, Patricia;Porazinski, Sean;Ladomery, Michael R.
癌基因ETS相关基因（ERG）编码一种转录因子，在造血、血管生成、血管发生、炎症、迁移和侵袭中发挥作用。ERG癌基因在>50%的前列腺癌病例中被激活，通常通过与跨膜蛋白酶丝氨酸2的雄激素应答启动子的基因融合。磷酸酶和张力蛋白同源物（PTEN）是一种重要的肿瘤抑制基因，在癌症中经常失活。ERG过表达与PTEN失活或丢失相结合通常与侵袭性前列腺癌相关。本研究旨在确定ERG是否直接调节PTEN转录。ERG被证明与PTEN启动子结合并抑制其转录。ERG过表达减少内源性PTEN表达，而ERG敲低增加PTEN表达。ERG抑制PTEN的能力可能有助于形成一个更允许癌症的环境。
The oncogene ETS-related gene (ERG) encodes a transcription factor with roles in the regulation of haematopoiesis, angiogenesis, vasculogenesis, inflammation, migration and invasion. The ERG oncogene is activated in >50% of prostate cancer cases, generally through a gene fusion with the androgen-responsive promoter of transmembrane protease serine 2. Phosphatase and tensin homologue (PTEN) is an important tumour suppressor gene that is often inactivated in cancer. ERG overexpression combined with PTEN inactivation or loss is often associated with aggressive prostate cancer. The present study aimed to determine whether or not ERG regulates PTEN transcription directly. ERG was demonstrated to bind to the PTEN promoter and repress its transcription. ERG overexpression reduced endogenous PTEN expression, whereas ERG knockdown increased PTEN expression. The ability of ERG to repress PTEN may contribute to a more cancer-permissive environment.