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首页> 外文期刊>Cancer letters >Blockade of store-operated Ca2+ entry inhibits hepatocarcinoma cell migration and invasion by regulating focal adhesion turnover
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Blockade of store-operated Ca2+ entry inhibits hepatocarcinoma cell migration and invasion by regulating focal adhesion turnover

机译：储存操作的Ca2 +进入的阻断作用通过调节粘着斑更新来抑制肝癌细胞的迁移和侵袭

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Store-operated Ca2+ entry (SOCE) is a main Ca2+ influx pathway controlling the intracellular Ca2+ concentration in normal hepatocytes and hepatocellular carcinoma (HCC) cells. Ca2+ influx has been demonstrated to be involved in liver oncogenesis. Stromal interacting molecule (STIM) 1 acts as a sensor for the level of Ca2+ stored in the endoplasmic reticulum, and Orai1 protein constitutes the pore-forming subunit of the store-operated channels. Recently, STIM1 and Orai1 were found critical for breast tumor cell migration and metastasis. However, the effects of Ca2+ influx pathway on migration and metastasis have not been studied in hepatocellular carcinoma. Here, we found that STIM1 had a higher expression in hepatoma tissues than in precancerous tissues of the same patients. In general, STIM expression is elevated in HCC cell lines compared to a normal hepatocyte cell line. HCC-LM3 cell, which has a higher migration ability, expresses five times higher level of STIM than other HCC cell lines. STIM1 could then be explored as a prognostic marker to screen liver cancer patients with high metastatic potential. Inhibition of SOCE and STIM1 enhance focal adhesions and decrease the focal adhesion turnover, suggesting the therapeutic potential of SOCE and STIM1 as new molecular targets for metastatic HCC. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
机译：存储操作的Ca2 +进入（SOCE）是控制正常肝细胞和肝细胞癌（HCC）细胞中细胞内Ca2 +浓度的主要Ca2 +流入途径。已经证实Ca 2+内流与肝癌发生有关。基质相互作用分子（STIM）1充当存储在内质网中Ca2 +水平的传感器，Orai1蛋白构成存储操作通道的成孔亚基。最近，发现STIM1和Orai1对乳腺癌细胞的迁移和转移至关重要。然而，尚未在肝细胞癌中研究Ca 2+流入途径对迁移和转移的影响。在这里，我们发现STIM1在肝癌组织中的表达高于同一患者的癌前组织。通常，与正常肝细胞系相比，HCC细胞系中的STIM表达升高。具有较高迁移能力的HCC-LM3细胞表达的STIM水平是其他HCC细胞系的五倍。然后可以将STIM1用作筛选具有高转移潜力的肝癌患者的预后指标。 SOCE和STIM1的抑制作用增强粘着斑并减少粘着斑周转，表明SOCE和STIM1作为转移性HCC的新分子靶标具有治疗潜力。 （C）2012 Elsevier Ireland Ltd.保留所有权利。

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