瘢痕疙瘩是一种病理性伤口愈合过程中形成的皮肤胶原性疾病。目前，我国瘢痕疙瘩发病率逐年升高，但无满意的治疗方法。研究瘢痕疙瘩的发病机制及治疗方法一直是皮肤科一个重要的研究领域。RUNX3基因是RUNX家族成员，在细胞的发育、凋亡、信号转导等细胞功能中起到重要作用。前期研究发现，RUNX3在瘢痕疙瘩组织中广泛高表达，且与增殖能力密切相关，提示RUNX3在瘢痕疙瘩的发生发展中起到重要作用，但其机制尚未明确。为了初步探明其机制，我们在预实验中通过基因芯片、RT-PCR等实验方法，发现RUNX3可调控Skp2表达。我们推测RUNX3可能是通过Skp2调控瘢痕疙瘩的发生发展。基于以上内容，本项目拟研究RUNX3/Skp2蛋白在瘢痕疙瘩增殖、凋亡、周期进程等生物学功能中的作用及调节机制，填补瘢痕疙瘩与RUNX3蛋白相关研究的空白，为瘢痕疙瘩的临床治疗提供有效的分子靶点及标志物。

Keloid is the formation of a type of scar which, depending on its maturity. To date, there is no effective therapies for keloid, and its pathogenesis still unknown. RUNX3 is the member of RUNX3 family, and it play important roles in cell growth, apoptosis and signal transduction. In our study, we found that RUNX3 was frequently overexpressed in keloid, and was highly related to keloid cell proliferation. These results indicate that RUNX3 play important roles in keloid development and progression. In order to identify the mechanism, we performed gene-microarray analysis and Real-time PCR, and found that RUNX3 could regulate Skp2 expression. Thus, we hypothesis that RUNX3 modulated keloid progression through regulating Skp2 expression. Base on these, we decided to find out the functions and mechanisms of RUNX3/Skp2 in keloid development and progression, to provide effective biomarker and target for therapy.