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ΔNp63 promotes stem cell activity in mammary gland development and basal-like breast cancer by enhancing Fzd7 expression and Wnt signaling

机译:ΔNp63通过增强Fzd7表达和Wnt信号传导促进乳腺发育和基底样乳腺癌中的干细胞活性

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摘要

Emerging evidence suggests that cancer is populated and maintained by tumor initiating cells (TICs) with stem-like properties similar to that of adult tissue stem cells. Despite recent advances, the molecular regulatory mechanisms that may be shared between normal and malignant stem cells remain poorly understood. Here we show that the ΔNp63 isoform of the Trp63 transcription factor promotes normal mammary stem cell (MaSC) activity by increasing the expression of the Wnt receptor Fzd7, thereby enhancing Wnt signaling. Importantly, Fzd7-dependent enhancement of Wnt signaling by ΔNp63 also governs tumor initiating activity of the basal subtype of breast cancer. These findings establish ΔNp63 as a key regulator of stem cells in both normal and malignant mammary tissues and provide direct evidence that breast cancer TICs and normal MaSCs share common regulatory mechanisms.
机译:越来越多的证据表明,癌症是由具有与成人组织干细胞相似的干样特性的肿瘤起始细胞(TIC)形成和维持的。尽管有最新进展,但对于正常干细胞和恶性干细胞之间可能共有的分子调控机制仍然知之甚少。在这里,我们显示Trp63转录因子的ΔNp63亚型通过增加Wnt受体Fzd7的表达来促进正常的乳腺干细胞(MaSC)活性,从而增强Wnt信号传导。重要的是,ΔNp63依赖Wz信号的Fzd7依赖性增强也控制着乳腺癌基础亚型的肿瘤启动活性。这些发现将ΔNp63确立为正常和恶性乳腺组织中干细胞的关键调节剂,并提供直接证据证明乳腺癌TIC和正常MaSC具有共同的调节机制。

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