β-抑制蛋白1通过调节前列腺癌细胞中的GSK-3β/β-连环蛋白信号通路促进上皮-间质转化。
β-arrestin1 promotes epithelial-mesenchymal transition via modulating GSK-3β/β-catenin pathway in prostate cancer cells.
作者信息
Duan Xiaolu, Zhang Tao, Kong Zhenzhen, Mai Xin, Lan Chuangxin, Chen Dong, Liu Yang, Zeng Zhiwen, Cai Chao, Deng Tuo, Wu Wenqi, Zeng Guohua
机构信息
Department of Urology, Minimally Invasive Surgery Center, The First Affiliated Hospital of Guangzhou Medical University, Guangdong Key Laboratory of Urology, Guangzhou Institute of Urology, China.
Shenzhen Mental Health Center, Shenzhen Key Lab for Psychological Healthcare, China.
出版信息
Biochem Biophys Res Commun. 2016 Oct 14;479(2):204-210. doi: 10.1016/j.bbrc.2016.09.039. Epub 2016 Sep 9.
Recently, β-arrestin1 was indicated as a tumor promoter in prostate cancer, but its exact role in cancer metastasis still have not been well clarified. Here, our data revealed that β-arrestin1 could promote the migration and invasion of prostate cancer cells via initiating epithelial-mesenchymal transition (EMT). Mechanically, β-arrestin1 could increase the transcriptional activity and expression of β-catenin, together with Akt activity, whereas decrease the activities of GSK-3β and PP2A. In addition, β-arrestin1 could function as a scaffold protein in modulating the interactions between PP2A, Akt, GSK-3β and β-catenin. These results reveal a novel mechanism of β-arrestin1 in modulating EMT and GSK-3β/β-catenin signaling in prostate cancer, thereby suggest that assessment of β-arrestin1 may provide a potential therapeutic target for prostate cancer.
最近，β-抑制蛋白1被认为是前列腺癌中的一种肿瘤促进因子，但其在癌症转移中的确切作用仍未得到充分阐明。在此，我们的数据显示，β-抑制蛋白1可通过启动上皮-间质转化（EMT）来促进前列腺癌细胞的迁移和侵袭。机制上，β-抑制蛋白1可增加β-连环蛋白的转录活性和表达，同时增强Akt活性，而降低糖原合成酶激酶3β（GSK-3β）和蛋白磷酸酶2A（PP2A）的活性。此外，β-抑制蛋白1可作为一种支架蛋白，调节PP2A、Akt、GSK-3β和β-连环蛋白之间的相互作用。这些结果揭示了β-抑制蛋白1在调节前列腺癌EMT和GSK-3β/β-连环蛋白信号传导中的一种新机制，从而表明对β-抑制蛋白1的评估可能为前列腺癌提供一个潜在的治疗靶点。
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