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首页> 外文期刊>Cellular Signalling >PI3K/Akt to GSK3β/β-catenin signaling cascade coordinates cell colonization for bladder cancer bone metastasis through regulating ZEB1 transcription
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PI3K/Akt to GSK3β/β-catenin signaling cascade coordinates cell colonization for bladder cancer bone metastasis through regulating ZEB1 transcription

机译：PI3K / Akt至GSK3β/β-catenin信号传导级联可通过调节ZEB1转录来协调细胞定植，从而促进膀胱癌骨转移

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摘要

Muscle-invasive bladder cancer is associated with a high frequency of metastasis, and bone is the most common metastatic site outside the pelvis. To clarify its organ-specific characteristics, we generated a successive bone metastatic T24-B bladder cancer subline following tail vein injection of metastatic T24-L cells. Compared with parental T24-L cells, epithelial-like T24-B cells displayed increased adhesion but decreased migration or invasion abilities as well as up-regulation of cytokeratins and down-regulation of vimentin, N-cadherin and MMP2. Mechanically, phosphatidylinositol 3-kinase(PI3K)/Akt targets glycogen synthase kinase-3β(GSK3β)/β-catenin to control ZEB1 gene transcription, and then subsequently regulates the expression of cytokeratins, vimentin and MMP2. Importantly, ZEB1 is essential for bladder cancer invasion in vitro and distant metastasis in vivo, and ZEB1 overexpression was highly correlated with the expression of those downstream markers in clinical tumor samples. Overall, this study reveals a novel mechanism facilitating metastatic bladder cancer cell re-colonization into bone, and confirms the significance of mesenchymal-to-epithelial transition(MET)in formation of bone metastasis.
机译：肌肉浸润性膀胱癌与高转移率有关，而骨是骨盆外最常见的转移部位。为了阐明其器官特异性特征，我们在尾静脉注射转移性T24-L细胞后产生了连续的骨转移性T24-B膀胱癌亚系。与亲代T24-L细胞相比，上皮样T24-B细胞显示出增加的粘附性，但是降低了迁移或侵袭能力以及细胞角蛋白的上调和波形蛋白，N-钙粘蛋白和MMP2的下调。机械上，磷脂酰肌醇3-激酶（PI3K）/ Akt靶向糖原合酶激酶-3β（GSK3β）/β-catenin，以控制ZEB1基因的转录，然后调节细胞角蛋白，波形蛋白和MMP2的表达。重要的是，ZEB1对于膀胱癌的体外侵袭和体内远处转移至关重要，并且ZEB1的过表达与临床肿瘤样品中这些下游标志物的表达高度相关。总的来说，这项研究揭示了一种促进转移性膀胱癌细胞重新定植到骨中的新机制，并证实了间充质到上皮转化（MET）在骨转移形成中的重要性。

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