HSPC111异常表达及核糖体生物合成异常均与前列腺癌（PCa）的进展密切相关。我们研究发现HSPC111在PCa中显著高表达，且可通过调节细胞中rRNA的含量影响核糖体生物合成；此外，14种参与60S大亚基及15种参与40S小亚基组装的RPs在PCa中含量均显著增加。另有研究发现HSPC111参与30S及50S核糖体蛋白颗粒的组装。据此，我们推测：HSPC111可通过调节核糖体生物合成影响PCa进展。本项目以HSPC111为中心，核糖体应激为切入点，在进一步研究HSPC111调节核糖体生物合成的基础上重点研究：1) HSPC111异常表达调节rRNA剪切加工的机制；2) HSPC111通过调节RPs的表达及功能影响核糖体生物合成的机制；3) HSPC111在60S及40S大小亚基细胞核质转运过程中的作用及机制。以期阐明在PCa进展中HSPC111影响核糖体生物合成的分子机理。

Abnormal expression of HSPC111 and aberrant ribosomal biogenesis are associated with prostate cancer (PCa) development. We previously found that HSPC111 was highly expressed in PCa and that HSPC111 impacts ribosomal biogenesis through regulating intracellular rRNA content. Moreover, the content of 14 and 15 kinds of ribosomal proteins (RPs) that are involved in assembly of large (60S) and small (40S) subunits, respectively, are increased in PCa. Other groups demonstrated that HSPC111 act to facilitate synthesis/assembly of 30S- and 50S-ribosomal particles. In this regard, we hypothesize that HSPC111 plays a role in PCa development by regulating ribosomal biogenesis. The current study focuses on: 1) how abnormal expression of HSPC111 regulates rRNA sheering and processing; 2) the mechanism of HSPC111 influences ribosomal biogenesis by regulating RPs expression; 3) the role of HSPC111 in nuclear-cytoplasmic transport of large (60S) and small (40S) subunits and underlying mechanisms. We aim to elucidate the molecular pathogenesis of HSPC111-regulating ribosomal biogenesis in PCa development.