组织工程软骨种子细胞表型保持是目前的重要方向，Sox9为调控软骨细胞表型的核心因子。LncRNA在软骨分化中发挥重要作用，但其对Sox9的调控机制不详。在前期证实miR-145靶向调控Sox9基础上,高通量测序发现Lnc-32598在软骨分化中显著上调，且与Sox9竞争性结合miR-145；干扰该Lnc则Sox9蛋白和核酸均降低，这难以通过miR-145-Sox9单一转录后调控阐释，推测还存在针对Sox9转录水平的调控机制。质谱证据发现该Lnc可与FXR1结合，后者可募集STAT3结合到Sox9增强子，故提出Lnc-32598/FXR1/STAT3调控Sox9参与软骨分化假说。拟以Sox9的CeRNA调控网络为基础，通过体内外实验证实上述相关分子的表达规律，阐明Lnc对Sox9两种调控细节，并利用动物模型明确干预该Lnc路径对软骨修复的影响。本研究将为组织工程策略进行软骨修复提供理论指导。

The phenotype maintenance of seed cells in tissue engineered cartilage is the current focus. Sox9 is a key factor that regulates the phenotype of chondrocytes. LncRNA plays an important role in the chondrocyte differentiation. But its mechanism of regulation of Sox9 is unknown. In preliminary experiment，we had confirmed that miR-145 targeting Sox9. Through high-throughput sequencing, we found that Lnc-32598 was significantly up-regulated during chondrocyte differentiation and Lnc-32598 competed with Sox9 for binding to miR-145. After interfering the LncRNA expression, the Sox9 expression was reduced on both protein and mRNA level, which was difficult to be explained only by miR-145-Sox9 post-transcriptional regulation. These results suggest that there are other regulation manners for Sox9 on the transcriptional levels. Mass spectrometry evidence showed that the LncRNA was combined with FXR1 which recruited STAT3 to bind to the Sox9 enhancer, proposing Lnc-32598/FXR1/STAT3 regulation of Sox9 was involved in chondrocyte differentiation. This study tries to find out the potential ceRNA expression pattern of Lnc-32598 on the regulation of Sox9 by in vivo and in vitro experiments, and the effect of LncRNA pathway on cartilage repair will be confirmed by animal model. This study will provide theoretical guidance for cartilage repair performed by tissue engineering.