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首页> 外文期刊>Cell cycle >Turning the tables: Myc activates Wnt in breast cancer.
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Turning the tables: Myc activates Wnt in breast cancer.

机译：扭转局面：Myc激活乳腺癌中的Wnt。

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摘要

Previous molecular and genetic data implicate the c-myc gene as a critical downstream effector of the Wnt/TCF pathway in colon cancer. However, the involvement of c-myc in mammary epithelial cell transformation had not been explored. We recently showed that c-Myc induces a profound morphological transformation in human mammary epithelial cells accompanied by anchorage-independent growth. The mechanism of c-Myc transformation was revealed in part through the finding that, in contrast to colon cancer, c-Myc activates the Wnt pathway and endogenous TCF activity by suppressing the Wnt inhibitors DKK1 and SFRP1. Notably, DKK1 and SFRP1 were found to be strongly suppressed in human breast cancer cell lines, and their re-expression inhibited the transformed phenotype. We demonstrated that breast cancer cells become dependent on repression of the Wnt inhibitors for cell proliferation, i.e. they have acquired an "oncogene addiction", suggesting that the Myc-Wnt pathway is an attractive therapeutic target. We propose that a positive feedback loop of c-myc and Wnt signaling operates in breast cancer.
机译：先前的分子和遗传数据暗示c-myc基因是结肠癌Wnt / TCF途径的关键下游效应子。但是，尚未探讨c-myc在乳腺上皮细胞转化中的作用。我们最近表明c-Myc诱导人类乳腺上皮细胞发生深刻的形态转化，并伴随着锚定非依赖性生长。 c-Myc转化的机制在一定程度上揭示了这一发现：与结肠癌相反，c-Myc通过抑制Wnt抑制剂DKK1和SFRP1激活Wnt途径和内源性TCF活性。值得注意的是，发现DKK1和SFRP1在人乳腺癌细胞系中受到强烈抑制，并且它们的重新表达抑制了转化表型。我们证明乳腺癌细胞变得依赖于Wnt抑制剂抑制细胞增殖，即它们已获得“致癌基因成瘾”，这表明Myc-Wnt途径是有吸引力的治疗靶标。我们建议在乳腺癌中存在c-myc和Wnt信号的正反馈回路。

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