研究表明前列腺非可控性炎症（NCP）可转变为前列腺上皮内瘤变（PIN），但目前对此过程关键分子调控机制和规律仍然不清。我们前期研究显示mTOR在PIN表达明显比NCP高，提示mTOR的异常表达可能与PIN的发生发展相关。已有研究显示IL-6和自噬在NCP转变为PIN的过程中起重要作用；且IL-6通过mTOR信号通路调控炎症发生发展过程，提示NCP转变为PIN的机制可能是由IL-6/mTOR组成的分子网络调控的结果。因此，本项目以IL-6/mTOR为切入点，拟采用国际最新的PIN动物模型，针对PIN发生发展过程，运用分子生物学及动物模型等方法，构建NCP转变为PIN的动物模型；阐明IL-6 、mTOR和自噬在此过程中的作用；揭示IL-6在NCP转变为PIN过程中分子调控机制；构建其关键调控位点和信号通路，为PIN的防治提供新的策略与作用靶点。

It has demonstrated that non-controlled prostate inflammation (NCP) can change into prostatic intraepithelial neoplasia(PIN), however, little is known about the its key regulatory molecules mechanisms and regulation rules.We previously study show that mTOR in PIN markedly higher than NCP, this suggestion that the abnormal expression of mTOR relate with the development of PIN.it is also showed that IL-6 and autophagy are play an important role in the process of NCP change into PIN;and IL-6 through mTOR pathway regulate the development of inflammation, this suggestion that the mechanisms of NCP change into PIN result from molecular regulatory by IL-6/mTOR.So, We will intend to study breakthrough point of IL-6/mTOR,apply the new animal models of PIN,aim to the the process of PIN, constuct the animal models of NCP change into PIN; revealing the role of IL-6 、mTOR and autophagy in the NCP change into PIN;revealing its mechanisms of the molecular regulatory;constuct the key regulatorysites and signaling pathways in NCP change into PIN, to provide the new strategies and targets with the PIN.