SFRPs基因作为Wnt信号通路的抑制剂，在多种肿瘤的发生发展中起着重要作用。我们前期工作发现SFRPs在黑色素瘤中表达缺失，并可能受表观遗传学-DNA甲基化机制调控。本课题以SFRPs为研究目标，通过对细胞及组织中SFRPs启动子甲基化水平与该基因表达的关系来揭示黑色素瘤中SFRPs表达的表观遗传学调控机制，为黑色素瘤的早期诊断提供靶点；用去甲基化方法逆转因甲基化失活的SFRPs，为探索抗黑色素瘤治疗的新型药物奠定基础；建立SFRPs差异表达的稳定黑色素瘤细胞系及相对应移植瘤动物模型，分别从细胞和动物水平考察SFRPs差异表达后对黑色素瘤细胞增殖、凋亡等生物学特性的影响；深入探讨SFRPs对Wnt信号通路的影响及对细胞凋亡和周期的调控，以期揭示SFRPs甲基化在黑色素瘤发生发展的分子机制，为通过封闭特异的信号分子为黑色素瘤防治研究提供新的思路。

SFRPs gene as inhibitors of the Wnt signaling pathway plays an important role in a variety of tumor development. Our previous work found SFRPs expressing was absent in melanoma because of gene promoter methylation. In this research, we focus on SFRPS and will discover the relationship between SFRPs and methylation of SFRPs in cell and tissues to reveal the mechanisms of epigenetic regulation of SFRPs in melanoma, to provide targets for early diagnosis of melanoma; The demethylating method reversed inactivation SFRPs caused by methylation to exploring a new drugs against melanoma treatment. Establishing the stable melanoma cell lines with variable SFRPs expression and corresponding animal models, investigate the characteristics of the cell proliferation, apoptosis and other biological characteristics; we further try to determine the relationship between SFRPs and the Wnt signaling pathway, to reveal SFRPs methylation mechanism in melanoma development, thereby provides a new way for melanoma prevention and treatment though the silence of the specific signaling molecule.

Wnt信号通路促进黑色素瘤的发生和发展，SFRPs基因作为Wnt信号通路的抑制剂，在多种肿瘤的发生发展中起着重要作用。本课题发现SFRP2在人黑色素瘤组织中的表达减少，其甲基化表达增加。同时发现多株人黑色素瘤细胞中SFRP2表达下降，通过5-aza-dCyd进行去甲基化治疗后，SFRP2表达上升，证明其通过抑制黑色素瘤细胞β-catenin的核聚集，从而抑制黑色素瘤的侵袭作用。实验进一步在人黑色素瘤细胞株A375中通过高表达SFRP2水平，发现对细胞侵袭有明显影响，目前动物实验论证在进行中。目前实验证明SFRP2通过抑制Wnt信号通路从而抑制黑色素瘤的侵袭，SFRP2基因的甲基化可能影响黑色素瘤的发展。