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首页> 外文期刊>Journal of Cellular Physiology >Acute L-glutamine deprivation compromises VEGF-a upregulation in A549/8 human carcinoma cells.
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Acute L-glutamine deprivation compromises VEGF-a upregulation in A549/8 human carcinoma cells.

机译：急性谷酰胺VEGF-a剥夺妥协upregulation A549/8人类细胞癌。

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摘要

Tumor ischemia participates in angiogenesis and cancer progression through cellular responses to hypoxia and nutrient deprivation. However, the contribution of amino acids limitation to this process remains poorly understood. Using serum-free cell culture conditions, we tested the impact of L-glutamine deprivation on metabolic and angiogenic responses in A549/8 carcinoma cells. In these cells, lowering glutamine concentration modified the cell cycle distribution and significantly induced apoptosis/necrosis. Although glutamine deprivation led to a HIF-independent increase in VEGF-A mRNA, the corresponding protein level remained low and correlated with the inhibition of protein synthesis and activation of the GCN2/eIF2alpha pathway. Limitation of glutamine availability also hampers hypoxia- and hypoglycemia-induced VEGF-A protein upregulation. Thus, glutamine deprivation may have no direct effect on VEGF-dependent angiogenesis, compared to hypoxia or to glucose deprivation, and may instead be detrimentalto cancer progression by antagonizing ischemia-induced stresses.
机译：参与血管生成和肿瘤缺血程度通过细胞应对癌症恶化缺氧和营养不足。贡献氨基酸的限制过程仍然知之甚少。无血清细胞培养条件下,我们测试了谷酰胺剥夺对代谢的影响并在A549/8癌血管生成反应细胞。细胞周期集中修改分布和显著诱导细胞凋亡/坏死。剥夺导致HIF-independent增加VEGF-A mRNA,相应的蛋白质水平保持在低位,与抑制蛋白质的合成和激活的GCN2 / eIF2alpha通路。也阻碍了缺氧-和可用性hypoglycemia-induced upregulation VEGF-A蛋白质。因此,谷氨酰胺剥夺可能没有直接影响VEGF-dependent血管生成,相比缺氧或葡萄糖剥夺和可能而不是被detrimentalto癌症恶化得罪ischemia-induced压力。

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