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首页> 外文期刊>Journal of Cellular Physiology >Wnt/beta-catenin signaling pathway and thioredoxin-interacting protein (TXNIP) mediate the 'glucose sensor' mechanism in metastatic breast cancer-derived cells MDA-MB-231.
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Wnt/beta-catenin signaling pathway and thioredoxin-interacting protein (TXNIP) mediate the 'glucose sensor' mechanism in metastatic breast cancer-derived cells MDA-MB-231.

机译：Wnt /β-连环蛋白信号通路thioredoxin-interacting蛋白(TXNIP)调解转移性的“葡萄糖传感器”机制cancer-derived乳腺癌mda - mb - 231细胞。

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In this study we investigated the effect of glucose on GSK3beta and beta-catenin expression and the involvement of the N-linked glycosylation and hexosamine pathways in the Wnt canonical pathway in response to in vitro conditions resembling normoglycemia (5 mmol) and hyperglycemia (20 mmol) in the metastatic breast cancer-derived cell line MDA-MB-231. We also investigated the relationship between this circuitry and the thioredoxin-interacting protein (TXNIP) regulation that seems to be related. MDA-MB-231 cells were grown either in 5 or 20 mM glucose chronically prior to plating. For glucose shift (5/20), cells were plated in 5 mM glucose and shifted to 20 mM at time 0. Both protein and mRNA levels for GSK3beta but only the protein expression for beta-catenin, were increased in response to high glucose. Furthermore, we assessed the response of GSK3beta, beta-catenin, and TXNIP to inhibition of the N-linked glycosylation, hexosamine, and Wnt pathways. Wnt signaling pathway activation was validated by specific reporter assay. We show that high levels of glucose regulate mRNA and protein expression of GSK3beta, and consequently higher levels of activated beta-catenin protein, which locates to the nucleus and is associated with increased levels of cyclin D1 expression. This event coincides with increased level of N-terminal Ser 9 phosphorylation of GSK3beta protein. The inhibition of both the hexosamine pathway and N-linked glycosylation along with Wnt signaling pathway by sFRP1 and DKK1 is associated with significant decrease of the protein levels of GSK3beta, beta-catenin, and TXNIP RNA. Our work illuminates a novel and never described before function of this signaling pathway that relates glucose metabolism with redox regulation mechanism.
机译：在这项研究中,我们调查的影响葡萄糖GSK3beta和β-连环蛋白表达的参与N-linked糖基化并在Wnt规范己醣胺通路在体外反应条件下路径像normoglycemia(5更易)高血糖在转移性乳腺癌(20更易)cancer-derived细胞系mda - mb - 231。之间的关系进行了研究电路和thioredoxin-interacting蛋白质(TXNIP)监管,似乎是相关的。mda - mb - 231细胞生长在5或20毫米葡萄糖在电镀之前长期。转变(5/20),细胞被镀在5毫米葡萄糖和转移到20毫米在时刻0。mRNA水平GSK3beta但只有蛋白质为β-连环蛋白表达增加应对高葡萄糖。评估GSK3beta的反应,β-连环蛋白,和TXNIP N-linked的抑制糖基化、氨基己醣和Wnt通路。信号通路激活验证了特定的记者分析。葡萄糖调节mRNA和蛋白的表达GSK3beta,因此更高水平的激活β-连环蛋白的定位细胞核和增加有关水平的细胞周期蛋白D1的表情。恰逢增加氨基端Ser的水平9 GSK3beta蛋白质的磷酸化。己醣胺通路和抑制N-linked糖基化和Wnt信号通路sFRP1和DKK1是相关联的蛋白质含量的显著下降GSK3beta、β-连环蛋白和TXNIP RNA。照亮一个小说,以前从来没有描述这个信号通路相关的函数葡萄糖代谢与氧化还原调控机制。

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