Lungs for Living Research Centre, UCL Respiratory, University College London, London, United Kingdom.
Lungs for Living Research Centre, UCL Respiratory, University College London, London, United Kingdom; Department of Environmental, Biological, and Pharmaceutical Sciences and Technologies, University of Campania Luigi Vanvitelli, Caserta, Italy.
J Biol Chem. 2021 Nov;297(5):101223. doi: 10.1016/j.jbc.2021.101223. Epub 2021 Sep 29.
Malignant pleural mesothelioma (MPM) is a rare, aggressive, and incurable cancer arising from the mesothelial lining of the pleura, with few available treatment options. We recently reported that loss of function of the nuclear deubiquitinase BRCA1-associated protein 1 (BAP1), a frequent event in MPM, is associated with sensitivity to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis. As a potential underlying mechanism, here we report that BAP1 negatively regulates the expression of TRAIL receptors: death receptor 4 (DR4) and death receptor 5 (DR5). Using tissue microarrays of tumor samples from MPM patients, we found a strong inverse correlation between BAP1 and TRAIL receptor expression. BAP1 knockdown increased DR4 and DR5 expression, whereas overexpression of BAP1 had the opposite effect. Reporter assays confirmed wt-BAP1, but not catalytically inactive BAP1 mutant, reduced promoter activities of DR4 and DR5, suggesting deubiquitinase activity is required for the regulation of gene expression. Co-immunoprecipitation studies demonstrated direct binding of BAP1 to the transcription factor Ying Yang 1 (YY1), and chromatin immunoprecipitation assays revealed BAP1 and YY1 to be enriched in the promoter regions of DR4 and DR5. Knockdown of YY1 also increased DR4 and DR5 expression and sensitivity to TRAIL. These results suggest that BAP1 and YY1 cooperatively repress transcription of TRAIL receptors. Our finding that BAP1 directly regulates the extrinsic apoptotic pathway will provide new insights into the role of BAP1 in the development of MPM and other cancers with frequent BAP1 mutations.
恶性胸膜间皮瘤 (MPM) 是一种罕见的侵袭性和不可治愈的癌症,起源于胸膜的间皮细胞层,治疗选择有限。我们最近报道,核去泛素化酶 BRCA1 相关蛋白 1 (BAP1) 的功能丧失,这是 MPM 中的一个常见事件,与肿瘤坏死因子相关凋亡诱导配体 (TRAIL) 介导的细胞凋亡的敏感性有关。作为一种潜在的潜在机制,我们在这里报告 BAP1 负调节 TRAIL 受体的表达:死亡受体 4 (DR4) 和死亡受体 5 (DR5)。使用来自 MPM 患者肿瘤样本的组织微阵列,我们发现 BAP1 与 TRAIL 受体表达之间存在强烈的负相关。BAP1 敲低增加了 DR4 和 DR5 的表达,而 BAP1 的过表达则产生相反的效果。报告基因实验证实 wt-BAP1,但不是催化失活的 BAP1 突变体,降低了 DR4 和 DR5 的启动子活性,表明去泛素化酶活性是基因表达调控所必需的。共免疫沉淀研究表明 BAP1 与转录因子 Ying Yang 1 (YY1) 直接结合,染色质免疫沉淀实验显示 BAP1 和 YY1 富集在 DR4 和 DR5 的启动子区域。YY1 的敲低也增加了 DR4 和 DR5 的表达和对 TRAIL 的敏感性。这些结果表明 BAP1 和 YY1 协同抑制 TRAIL 受体的转录。我们发现 BAP1 直接调节外源性凋亡途径,这将为 BAP1 在 MPM 和其他频繁发生 BAP1 突变的癌症的发展中的作用提供新的见解。