前期研究发现PPARγ能抑制肝癌的生成，但其同族PPARβ在许多肿瘤生成中却显示出致癌作用，且PPARβ在肝癌中的作用仍存在着许多争议。本项目拟运用荧光定量PCR验证PPARβ mRNA表达在肝癌组织中是否升高。通过体外肝癌和正常肝细胞培养，转染siRNA或pcDNA3.1使PPARβ基因敲除或过表达，以MTS、流式细胞仪、细胞侵袭转移实验等方法检测PPARβ对肝癌细胞增长、凋亡、周期、癌细胞侵袭力及运动活力的作用。并建立PPARβ基因敲除小鼠及裸鼠成瘤两种动物模型进一步证实其作为致癌基因促进肿瘤的发生发展。且通过染色体免疫共沉淀和高通量测序技术的结合（ChIP-Seq）检测筛选PPARβ调控的下游基因，深入探讨其致癌的作用机制，探索其与其他相关基因的调控关系和信号通路。研究结果将为临床肝癌的基因治疗提供新的思路。

Previous study demonstrated that PPARγ inhibited hepatocellular carcinoma (HCC) development, while its family member PPARβ has been shown to promote tumorigenesis in many types of cancers. But the role of PPARβ in hepatocarcinogenesis remains controversial. We aim to investigate the tumorigenetic role of PPARβ in HCC. The mRNA expression of PPARβ in paired tissue samples from primary liver cancer and adjacent nontumor sites will be detected by real-time PCR. The effects of PPARβ on HCC or immortalized liver cell growth，apoptosis, invasion and migration will be examined using siRNA against PPARβ or PPARγ-expressing pcDNA3.1 vector. Both xenograft and PPARβ null mice models will be established to further prove the impact effect of PPARβ on the growth of liver cancer. Furthermore, the molecular basis of PPARβ function in hepatocarcinogenesis will be identified by cDNA expression array. PPARβ direct binding targets will be determined by chromosome immunoprecipitation (ChIP)-sequence.This study will help to better understand the role of PPARβ in hepatic tumorigenesis and provide a potential therapeutic assay for liver cancer through modulating PPARβ.