期刊
ANATOMICAL RECORD-ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY
卷 295, 期 12, 页码 2104-2113出版社
WILEY-BLACKWELL
DOI: 10.1002/ar.22592
关键词
teratocarcinoma; embryonic carcinoma cells; beta-catenin; C-myc; proliferation
资金
- National Natural Science Foundation of China [30871405, 30971653]
- Natural Science Foundation of Shandong Province [ZR2009CM018]
Aberrant activation of the Wnt/beta-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/beta-catenin signaling on the pathogenesis of teratocarcinoma, we used the mouse teratocarcinoma P19 cell line as a model in vitro. Gsk3 beta specific inhibitor (SB216763) was used to activate Wnt/beta-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 beta-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/beta-catenin signaling and induced P19 cell differentiation. In conclusion, activation of the Wnt/beta-catenin pathway could promote the proliferation and inhibit the differentiation of mouse teratocarcinoma cells by upregulation of c-myc expression. Anat Rec, 295:2104-2113, 2012. (C) 2012 Wiley Periodicals, Inc.
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