蛋白质精氨酸甲基转移酶PRMT1介导精氨酸甲基化修饰，在多种肿瘤中异常表达。C/EBPα作为一个重要的转录因子在组织特异性基因表达和细胞增殖中发挥着重要的调控功能。PRMT1是否能够修饰C/EBPα并且参与乳腺癌细胞的生长调控是一个重要而有趣的问题。我们前期研究发现， C/EBPα明显抑制MDA-MB-231乳腺癌细胞系的增殖。PRMT1可以直接修饰C/EBPα并且影响其靶基因调控区的染色质开放程度以及HDACs相关的抑制复合物和Brm依赖的SWI/SNF染色质重塑复合物的募集，进而而调节其转录活性。因此，本项目拟深入研究PRMT1特异修饰C/EBPα的分子机制，探讨C/EBPα的精氨酸甲基化修饰调控靶基因的染色质重塑机制；为阐明PRMT1介导的C/EBPα甲基化对肿瘤抑制作用的机制提供新的思路，为PRMT1-C/EBPα通路相关肿瘤治疗提供新的靶点。

PRMT1 is a major arginine methyltransferase in mammalian cells. Aberrent expression of PRMT1 is often observed in tumors. C/EBPα is an essential transcription factor involved in regulating tissue-specific gene expression and cancer cell proliferation. It is an important and interesting question whether C/EBPα is modified by PRMT1 and involved in regulation of breast cancer cell proliferation. Our previous data revealed C/EBPα, as transcription factor, could directly repress the expression of c-Fos, c-Myc and Cyclin D1 in MDA-MB-231 cells, PRMT1 was obviously upregulated in breast cancer clinical samples and cell lines, and loss of PRMT1 led to cellular growth arrest accompanied by the expression changes of several proliferation related genes. Most importantly, we further found PRMT1 interacted with and methylated C/EBPα, and methylation of C/EBPα resulted in impaired transcriptional activity. Therefore, the application aims to more deeply research on the target genes and molecular mechanisms of PRMT1 and C/EBPα on breast cancer proliferation, to explore the function of PRMT1-mediated methylation of C/EBPα in breast cancer cells.