类固醇受体共活化因子3（SRC-3）作为新受关注的癌因子，以SRC-3组蛋白乙酰化转录复合物（SRC-3/NR/p300/HDAC1）形式调控下游靶基因转录，同时发现类泛素蛋白（small ubiquitin-related modifier protein, SUMO）修饰可调控此转录复合物活性.SPOP异常引起SRC-3表达及SUMO化异常与恶性肿瘤发生密切相关。藤黄酸是一种高效低毒的抗肿瘤天然药物，前期实验中我们发现藤黄酸可下调SRC-3，推测藤黄酸可通过调控淋巴瘤中SPOP表达直接或间接调节SRC-3 的SUMO化，从而调节SRC-3组蛋白乙酰化转录复合物活性。本课题以B细胞-非霍奇金淋巴瘤为研究对象，深入探讨淋巴瘤中SPOP及SRC-3 SUMO化状态与转录复合物的活性的关系，并以此通路为靶点探讨藤黄酸的作用机理，为淋巴瘤的治疗寻找新的药物。

As a new oncogene,SRC-3 has been verified could control the transcriptional activity of downstream gene targets through SRC-3 histone actylation transcription complexes(SRC-3/NR/HAT/HDAC1), meanwhile, it was also discovered SUMO (smallubiquitin-related modifier protein,SUMO)modification could affect the stability of SRC-3/NR/HAT/HDAC complexes. The anomalous SUMO junction of SRC-3/NR/HAT/HDAC complexes，especially, the anomalous SUMO junction of SRC-3 was closely associated with tumorigenesis. Gambogic acid is a natural product with high-efficiency and low-toxicity. In past years, our group has verified that gambogic acid could down-regulate the protein and mRNA levels of SRC-3. After serious consideration about our results and others, we suggested that gambogic acid could probably control the SUMO junction of SRC-3 through regulation of enzymes about SUMO conjugation. By this way, gambogic acid could alter the stability of SRC-3 histone actytion translation complexes. This study aim to determine the function of SUMO modification of SRC-3/NR/HAT/HDAC complexes in B-NHL(B-cell-Non-Hodgkin's Lymphoma, B-NHL) and how gambogic acid regulates the SUMO midification of SRC-3. Meanwhile the role of the regulation mechanism of gambogic acid in anti-lymphoma will be explored which will provide new breakthrough for the treatment of B-NHL.