同源盒基因1（sine oculis homeobox 1, SIX1）在癌症的发生发展中起着关键作用，已经逐步成为目前热门的抗癌靶标。但SIX1作为转录因子，直接靶向成药的难度较高。为了阻断SIX1的促癌作用，本课题旨在SIX1的翻译后修饰水平寻找新的干预靶点。利用免疫共沉淀和生物质谱分析方法，我们初步鉴定出SIX1共调节蛋白SENP3（SUMO特异蛋白酶3）。利用多层次的技术手段，我们进一步发现SENP3可能通过干预SIX1的类泛素化过程和增强SIX1的转录因子活性调控前列腺癌的生长。本研究旨在证明这个假说，为前列腺癌的治疗提供新的治疗靶点，并为新一代的药物研发提供依据。

Sine oculis homeobox 1(SIX1) plays a critical role in the development and progression of multiple cancers, which renders it became a hot anticancer-target nowadays. However, as a transcription factor, SIX1 is difficult to be directly targeted. In order to block the pro-tumor effect of SIX1, this study aims to discover new targets based on the level of post-translational modification of SIX1. We preliminary identified SENP3(SUMO specific protease 3) as a novel co-regulator of SIX1 by the use of Co-IP and Biomass analysis. Using multiple biomedical methods, we further found that SENP3 may promote the growth of prostate cancer via intervening the SUMOylation and transcriptional activity of SIX1. The current study aims to prove this hypothesis and provides a novel target and new generation chemicals to treat prostate cancer.