标题：Wnt/β-Catenin Signaling Pathway Upregulates c-Myc Expression to Promote Cell Proliferation of P19 Teratocarcinoma Cells
作者机构：[Zhang, S] Department of Histology and Embryology, School of Medicine, Shandong University, Jinan 250012, China;[ Li, Y] Department of Histology and E 更多
通讯作者地址：[Hao, J]Shandong Univ, Sch Med, Dept Histol & Embryol, Jinan 250012, Peoples R China.
来源：The anatomical record: advances in integrative anatomy and evolutionary biology
关键词：β-catenin;C-myc;Embryonic carcinoma cells;Proliferation;Teratocarcinoma
摘要：Aberrant activation of the Wnt/β-catenin signaling pathway is a common event in human tumor progression. Wnt signaling has also been implicated in maintaining a variety of adult and embryonic stem cells by imposing a restraint to differentiation. To understand the function and mechanism of Wnt/β-catenin signaling on the pathogenesis of teratocarcinoma, we used the mouse teratocarcinoma P19 cell line as a model in vitro. Gsk3β specific inhibitor (SB216763) was used to activate Wnt/β-catenin signaling. All trans-retinoic acid (RA) was used to induce P19 cell differentiation. At different culture times, gene expression was examined by immunofluorescence staining, quantitative real-time PCR, and Western-blotting; BrdU incorporation assays were performed to measure P19 cell proliferation. Small interference RNA technology was used to downregulate c-myc expression. The results showed that SB216763 induced the nuclear translocation of β-catenin, upregulated the expression of c-myc and pluripotency related genes, oct4, sox2 and nanog, and blocked cell differentiation induced by all trans-RA. The proliferation of P19 cells was significantly enhanced by SB216763, as well as c-myc overexpression. C-myc downregulation inhibited P19 cell proliferation caused by activation of Wnt/β-catenin signaling and induced P19 cell differentiation. In conclusion, activation of the Wnt/β-catenin pathway could promote the proliferation and inhibit the differentiation of mouse teratocarcinoma cells by upregulation of c-myc expression.