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B-CATENIN SIGNALING PATHWAY AND THE TOLERANCE OF BREAST CANCER CELLS TO HYPOXIC CONDITIONS

机译:B-catenin信号传导途径和乳腺癌细胞对缺氧条件的耐受性

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摘要

We have previously shown that Snail, a regulator ofepithelial-mesenchymal transition, is activated in the hypoxia-resistant breast cancer cell line HBL-100. The purpose of this study was to evaluate the role offi-catenin signaling pathway in the maintenance of breast cancer cells' tolerance to hypoxia. The breast cancer cell lines MCF- 7 and HBL-100 were used in this study; HBL-100 cells were characterized by increased resistance to hypoxia. We have demonstrated that the transcription factor fi-catenin is activated in hypoxic conditions and the fi-catenin activity is supported by Snail, a regulator of epithelial-mesenchymal transition. The activated fi-catenin regulates the expression of genes of the cell response to hypoxia and thus, it maintains the growth of breast cancer in the reduced oxygen conditions. The coordinated activation of Snail/beta-catenin/HlF-la proteins in cell may be considered as an important factor of tumor resistance to hypoxia.
机译:我们之前已经表明,蜗牛是一种稳压剂的间充质转换,在缺氧乳腺癌细胞系HBL-100中被激活。 本研究的目的是评估在维持乳腺癌细胞对缺氧的耐受性中的脱硫信号传导途径的作用。 本研究使用乳腺癌细胞系MCF-7和HBL-100; 通过增加对缺氧的耐药性增加HBL-100细胞。 我们已经证明,转录因子Fi-Catenin在缺氧条件下激活,并且通过蜗牛支撑Fi-catenin活性,其上皮 - 间充质转换的调节剂。 活化的FI-Catenin调节细胞反应基因的表达对缺氧,因此,它保持乳腺癌在降低的氧气条件下的生长。 细胞中蜗牛/β-连环蛋白/ HLF-la蛋白的协调活化可被认为是肿瘤抗缺氧的重要因素。

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