Kappel Sven, Marques Ines Joao, Zoni Eugenio, Stokłosa Paulina, Peinelt Christine, Mercader Nadia, Kruithof-de Julio Marianna, Borgström Anna
1Institute of Biochemistry and Molecular Medicine, NCCR TransCure, University of Bern, Bern, Switzerland.
2Institute of Anatomy, University of Bern, Bern, Switzerland.
Curr Mol Biol Rep. 2017;3(4):208-217. doi: 10.1007/s40610-017-0072-8. Epub 2017 Oct 28.
Store-operated calcium entry (SOCE) is dysregulated in prostate cancer, contributing to increased cellular migration and proliferation and preventing cancer cell apoptosis. We here summarize findings on gene expression levels and functions of SOCE components, stromal interaction molecules (STIM1 and STIM2), and members of the Orai protein family (Orai1, 2, and 3) in prostate cancer. Moreover, we introduce new research models that promise to provide insights into whether dysregulated SOCE signaling has clinically relevant implications in terms of increasing the migration and invasion of prostate cancer cells.
Recent reports on Orai1 and Orai3 expression levels and function were in part controversial probably due to the heterogeneous nature of prostate cancer. Lately, in prostate cancer cells, transient receptor melastatin 4 channel was shown to alter SOCE and play a role in migration and proliferation. We specifically highlight new cancer research models: a subpopulation of cells that show tumor initiation and metastatic potential in mice and zebrafish models.
This review focuses on SOCE component dysregulation in prostate cancer and analyzes several preclinical, cellular, and animal cancer research models.
在前列腺癌中，钙库操纵性钙内流（SOCE）失调，导致细胞迁移和增殖增加，并抑制癌细胞凋亡。我们在此总结前列腺癌中SOCE组分、基质相互作用分子（STIM1和STIM2）以及Orai蛋白家族成员（Orai1、2和3）的基因表达水平及功能的相关研究结果。此外，我们介绍了一些新的研究模型，这些模型有望为失调的SOCE信号通路在促进前列腺癌细胞迁移和侵袭方面是否具有临床相关意义提供见解。
近期关于Orai1和Orai3表达水平及功能的报道部分存在争议，这可能是由于前列腺癌的异质性。最近，在前列腺癌细胞中，瞬时受体电位M型4通道被证明可改变SOCE，并在迁移和增殖中发挥作用。我们特别强调了新的癌症研究模型：在小鼠和斑马鱼模型中显示出肿瘤起始和转移潜能的细胞亚群。
本综述聚焦于前列腺癌中SOCE组分的失调，并分析了几种临床前、细胞和动物癌症研究模型。
