去泛素化酶OTUD6A调节c-Myc稳定性在前列腺癌代谢重塑中的机制研究

泛素-蛋白酶体系统介导细胞内蛋白质的降解过程，其中，泛素化与去泛素化的平衡起着至关重要的作用。通过生物信息学分析，我们发现去泛素化酶OTUD6A基因在前列腺癌中特异性地扩增，但OTUD6A蛋白质在前列腺癌发生发展中的作用机制并不清楚。我们的初步结果提示：1）OTUD6A在人前列腺癌中高表达，可能是一个原癌基因；2）OTUD6A敲低降低前列腺癌细胞体外成瘤性；3）OTUD6A可能通过去泛素化稳定c-Myc，引起肿瘤细胞代谢重塑。为进一步明确OTUD6A在前列腺癌的作用，本研究拟通过体内及体外实验，揭示OTUD6A通过去泛素化c-Myc，引起前列腺癌细胞代谢重塑及肿瘤发生发展的作用及分子机制，为寻找有效的药物作用靶点和治疗策略提供新线索。

The ubiquitin-proteasome system mediates the degradation of intracellular proteins, in which the balance between ubiquitination and deubiquitination plays a crucial role. Using bioinformatic analysis, we found that the OTUD6A gene is specifically amplified in prostate cancer. However, the role of OTUD6A in the development of prostate cancer is unclear. Our preliminary results suggest that: 1）OTUD6A is highly expressed in human prostate cancer and it might be a proto-oncogene; 2）Depletion of OTUD6A decreases the tumorigenesis of prostate cancer cell in vitro; 3）OTUD6A stimulates metabolic remodeling of tumor cells possibly through deubiquitinating and stabilizing c-Myc. To further clarify the role of OTUD6A in prostate cancer, using in vitro and in vivo experiments, this study aims to explore the role of OTUD6A in inducing metabolic remodeling and tumorigenesis of prostate cancer through deubiquitinating c-Myc, providing new clues for potential drug targets and treatment strategies.