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碳酸酐酶 IX 的抑制导致肿瘤细胞异常黏附焦点形成和侵袭能力下降。

Suppression of carbonic anhydrase IX leads to aberrant focal adhesion and decreased invasion of tumor cells.

机构信息

Institute of Virology, Department of Molecular Medicine, Slovak Academy of Sciences, 845 05 Bratislava, Slovak Republic.

出版信息

Oncol Rep. 2013 Mar;29(3):1147-53. doi: 10.3892/or.2013.2226. Epub 2013 Jan 4.

DOI:10.3892/or.2013.2226
PMID:23291973
Abstract

Carbonic anhydrase IX (CA IX) is a well-recognized hypoxia marker with promising diagnostic and therapeutic value. CA IX regulates the pH in hypoxic tumor cells and, thereby, contributes to microenvironmental acidosis and cell migration. To gain a better insight into the molecular processes driven by CA IX, we performed gene expression profiling of HT-1080 fibrosarcoma cells subjected to CA IX depletion by shRNA silencing. We identified the focal adhesion pathway as being significantly inhibited in the absence of CA IX and confirmed this finding by functional assays. Thus, we obtained the first direct evidence for the role of CA IX in focal adhesion.

摘要

碳酸酐酶 IX(CA IX)是一种公认的缺氧标志物,具有有前途的诊断和治疗价值。CAIX 调节缺氧肿瘤细胞中的 pH 值,从而有助于微环境酸中毒和细胞迁移。为了更好地了解 CA IX 驱动的分子过程,我们对 HT-1080 纤维肉瘤细胞进行了基因表达谱分析,这些细胞通过 shRNA 沉默被 CA IX 耗尽。我们发现,在没有 CA IX 的情况下,焦点黏附途径受到显著抑制,并通过功能测定证实了这一发现。因此,我们获得了 CA IX 在焦点黏附中的作用的第一个直接证据。

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