Lin Ling, Zhang Jian-Hua, Panicker Leelamma M, Simonds William F
Metabolic Diseases Branch, Building. 10 Room 8C-101, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Proc Natl Acad Sci U S A. 2008 Nov 11;105(45):17420-5. doi: 10.1073/pnas.0710725105. Epub 2008 Nov 5.
Parafibromin is a tumor suppressor protein encoded by HRPT2, a gene recently implicated in the hereditary hyperparathyroidism-jaw tumor syndrome, parathyroid cancer, and a subset of kindreds with familial isolated hyperparathyroidism. Human parafibromin binds to RNA polymerase II as part of a PAF1 transcriptional regulatory complex. The physiologic targets of parafibromin and the mechanism by which its loss of function can lead to neoplastic transformation are poorly understood. We show here that RNA interference with the expression of parafibromin or Paf1 stimulates cell proliferation and increases levels of the c-myc proto-oncogene product, a DNA-binding protein and established regulator of cell growth. This effect results from both c-myc protein stabilization and activation of the c-myc promoter, without alleviation of the c-myc transcriptional pause. Chromatin immunoprecipitation demonstrates the occupancy of the c-myc promoter by parafibromin and other PAF1 complex subunits in native cells. Knockdown of c-myc blocks the proliferative effect of RNA interference with parafibromin or Paf1 expression. These experiments provide a previously uncharacterized mechanism for the anti-proliferative action of the parafibromin tumor suppressor protein resulting from PAF1 complex-mediated inhibition of the c-myc proto-oncogene.
副纤维瘤蛋白是一种由HRPT2编码的肿瘤抑制蛋白,HRPT2是一个最近与遗传性甲状旁腺功能亢进-颌骨肿瘤综合征、甲状旁腺癌以及一部分家族性孤立性甲状旁腺功能亢进家族相关的基因。人副纤维瘤蛋白作为PAF1转录调节复合物的一部分与RNA聚合酶II结合。目前对副纤维瘤蛋白的生理靶点及其功能丧失导致肿瘤转化的机制了解甚少。我们在此表明,RNA干扰副纤维瘤蛋白或Paf1的表达会刺激细胞增殖,并增加c-myc原癌基因产物的水平,c-myc原癌基因产物是一种DNA结合蛋白,也是公认的细胞生长调节因子。这种效应是由c-myc蛋白的稳定以及c-myc启动子的激活导致的,而c-myc转录暂停并未缓解。染色质免疫沉淀显示在天然细胞中副纤维瘤蛋白和其他PAF1复合物亚基占据了c-myc启动子。敲低c-myc可阻断RNA干扰副纤维瘤蛋白或Paf1表达所产生的增殖效应。这些实验为副纤维瘤蛋白肿瘤抑制蛋白的抗增殖作用提供了一种此前未被描述的机制,该机制是由PAF1复合物介导的对c-myc原癌基因的抑制作用所导致的。