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首页> 外文期刊>Cell cycle >Modification of survival pathway gene expression in human breast cancer cells by tetraiodothyroacetic acid (tetrac).
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Modification of survival pathway gene expression in human breast cancer cells by tetraiodothyroacetic acid (tetrac).

机译：四碘胸苷乙酸（tetrac）对人乳腺癌细胞中生存途径基因表达的修饰。

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Tetraiodothyroacetic acid (tetrac) inhibits the cellular actions of thyroid hormone initiated at the hormone receptor on plasma membrane integrin alphavbeta3. Via interaction with the integrin, tetrac is also capable of inhibiting the angiogenic effects of vascular endothelial growth factor and basic fibroblast growth factor. MDA-MB-231 cells are estrogen receptor-negative human breast cancer cells shown to be responsive to tetrac in terms of decreased cell proliferation. Here we describe actions initiated at the cell surface receptor by unmodified tetrac and nanoparticulate tetrac on a panel of survival pathway genes in estrogen receptor-negative human breast cancer (MDA-MB-231) cells. Nanoparticulate tetrac is excluded from the cell interior. Expression of apoptosis inhibitors XIAP (X-linked inhibitor of apoptosis) and MCL1 (myeloid cell leukemia sequence 1) was downregulated by nanoparticulate tetrac in these breast cancer cells whereas apoptosis-promoting CASP2 and BCL2L14 were upregulated by the nanoparticulate formulation. Unmodified tetrac affected only XIAP expression. Expression of the angiogenesis inhibitor thrombospondin 1 (THBS1) gene was increased by both formulations of tetrac, as was the expression of CBY1, a nuclear inhibitor of catenin activity. The majority of differentially regulated Ras-oncogene family members were downregulated by nanoparticulate tetrac. The latter downregulated expression of epidermal growth factor receptor gene and unmodified tetrac did not. Nanoparticulate tetrac has coherent anti-cancer actions on expression of differentially-regulated genes important to survival of MDA-MB-231 cells.
机译：四碘甲状腺乙酸（​​tetrac）抑制在质膜整联蛋白alphavbeta3上的激素受体处起始的甲状腺激素的细胞作用。通过与整联蛋白的相互作用，tetrac还能够抑制血管内皮生长因子和碱性成纤维细胞生长因子的血管生成作用。 MDA-MB-231细胞是雌激素受体阴性的人类乳腺癌细胞，在降低细胞增殖方面显示出对tetrac的反应。在这里，我们描述了雌激素受体阴性的人类乳腺癌（MDA-MB-231）细胞中生存路径基因面板上未修饰的tric和纳米微粒tric在细胞表面受体处引发的动作。纳米微粒tetrac被排除在细胞内部。纳米微粒tetrac下调了这些乳腺癌细胞中凋亡抑制剂XIAP（X连锁凋亡抑制剂）和MCL1（髓样细胞白血病序列1）的表达，而促进凋亡的CASP2和BCL2L14则被纳米微粒制剂上调了。未经修饰的tetrac仅影响XIAP表达。两种tric制剂均增加了血管生成抑制剂血小板反应蛋白1（THBS1）基因的表达，而连环蛋白活性的核抑制剂CBY1的表达也有所增加。大部分差异调节的Ras致癌基因家族成员均被纳米微粒四环素下调。后者下调了表皮生长因子受体基因的表达，而未修饰的tetrac则没有。纳米微粒tetrac对差异表达基因的表达具有连贯的抗癌作用，该基因对MDA-MB-231细胞的存活至关重要。

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