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HIG2 通过缺氧依赖和非依赖途径促进结直肠癌进展。

HIG2 promotes colorectal cancer progression via hypoxia-dependent and independent pathways.

机构信息

Departments of Cancer Biology, The University of Texas MD Anderson Cancer Center, Houston, TX 77054, United States.

出版信息

Cancer Lett. 2013 Dec 1;341(2):159-65. doi: 10.1016/j.canlet.2013.07.028. Epub 2013 Aug 2.

Abstract

HIG2 (hypoxia-inducible gene 2) is a biomarker of hypoxia and elevated in several cancers. Here, we show that HIG2 also upregulated HIF-1α expression under hypoxic conditions and enhanced AP-1 expression under normoxic conditions, which affects colorectal cancer cell survival. Importantly, over-expression of HIG2 promoted tumor growth by suppressing apoptosis in a mouse orthotopic model. These results are likely relevant to human disease since we found that the expression of HIG2 is gradually elevated as tumors progress. Collectively, these findings suggest that HIG2 plays an important role in promoting colorectal cancer growth in hypoxia-dependent and independent manners.

摘要

HIG2(缺氧诱导基因 2)是缺氧的生物标志物,在多种癌症中升高。在这里,我们表明 HIG2 在缺氧条件下还上调 HIF-1α 的表达,并在常氧条件下增强 AP-1 的表达,从而影响结直肠癌细胞的存活。重要的是,HIG2 的过表达通过抑制小鼠原位模型中的细胞凋亡促进肿瘤生长。由于我们发现 HIG2 的表达随着肿瘤的进展逐渐升高,因此这些结果可能与人类疾病相关。总之,这些发现表明 HIG2 以缺氧依赖和非依赖的方式在促进结直肠癌细胞生长中发挥重要作用。

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