LAPTM4B/SPAG5在去势抵抗性前列腺癌进展中的作用及其调控机制的研究

已有研究表明，SPAG5可有效调控纺锤体的形成，在细胞有丝分裂过程中发挥极其重要的作用。项目组前期研究发现，SPAG5的表达水平在去势抵抗性前列腺癌进展过程中逐步上调。但SPAG5异常表达的调控机制并不明确。我们的前期预实验初步证实，LAPTM4B可与SPAG5发生相互作用，并能够进一步调控SPAG5的表达水平。项目组前期研究还发现，LAPTM4B与前列腺癌的进展密切相关。然而，LAPTM4B/SPAG5在去势抵抗性前列腺癌中的作用及机制，目前仍不清楚。为此，本项目拟在前期工作基础上，探讨LAPTM4B/SPAG5在去势抵抗性前列腺癌进展中的功能效应，并揭示其调控的分子机制。该研究的开展将为证实LAPTM4B/SPAG5可有效调控去势抵抗性前列腺癌进展的假设提供科学依据，为去势抵抗性前列腺癌发生的预防及治疗提供新的途径。

SPAG5 plays a very important role in cell mitosis by regulating mitotic spindle formation. Prvious study indicated that that SPAG5 expression level is drastically increased in primary prostate cancer (PCa) relative to normal samples, metastatic PCa samples relative to primary PCa, and castrate-resistant PCa (CRPC) relative to hormone naïve PCa, suggesting that SPAG5 can play an important role in PCa CRPC progression. In our previous study, we identified the LAPTM4B interacted with SPAG5 whose related to PCa progression. Furthermore, we found that LAPTM4B can influence the expression of SPAG5. Based on our previous work, we will focus on the regulation molecular mechanism of LAPTM4B/SPAG5 and its role in CRPC progression. Our study will provide both a further understanding to the evidence of the important role of LAPTM4B/SPAG5 in CRPC progression and a novel method to prevent and treat CRPC.