摘要
背景:血管内皮生长因子(VEGF)在多种肿瘤中高表达,包括胰腺癌。肿瘤细胞VEGF促进血管生成和肿瘤进展。然而,血管内皮生长因子在葡萄糖代谢中的作用尚不清楚。 目的:探讨血管内皮生长因子在胰腺癌细胞糖代谢中的作用及机制。 方法:胰腺癌细胞被165血管内皮生长因子刺激1到2小时。耗氧率(OCR)和细胞外酸化率(ECAR)使用海马XF96外流量分析仪测定。实时定量PCR检测糖酵解酶。神经纤毛蛋白1(NRP1)被shRNA诱导失活并探讨其VEGF诱导的糖酵解作用。免疫组织化学(IHC)进行中VEGF表达的相关性研究,αNRP1和缺氧诱导因子1(HIF-1α)在胰腺癌组织中的表达。 结果:VEGF刺激导致代谢线粒体氧化磷酸化糖酵解的胰腺癌转移。αHIF1α和NRP1蛋白水平均为血管内皮生长因子刺激后增加。NRP1表达下调降低胰腺癌细胞糖酵解。蛋白和VEGF水平与胰腺肿瘤组织中HIF1α表达。 结论:VEGF在胰腺癌细胞糖酵解增强通过α上调。NRP1在VEGF诱导的糖酵解过程中起着关键的作用。
关键词: 胰腺癌血管生成、血管再生术、糖酵解、VEGF、HIF1α
Current Molecular Medicine
Title:VEGF Promotes Glycolysis in Pancreatic Cancer via HIF1α Up-Regulation
Volume: 16 Issue: 4
Author(s): S. Shi, J. Xu, B. Zhang, S. Ji, W. Xu, J. Liu, K. Jin, D. Liang, C. Liang, L. Liu, C. Liu, Y. Qin, X. Yu
Affiliation:
关键词: 胰腺癌血管生成、血管再生术、糖酵解、VEGF、HIF1α
摘要: Background: Vascular endothelial growth factor (VEGF) is highly expressed in many types of tumors, including pancreatic cancer. Tumor cellderived VEGF promotes angiogenesis and tumor progression. However, the role of VEGF in glucose metabolism remains unclear.
Objective: We investigated the role and the underlying mechanism of VEGF in the glucose metabolism of pancreatic cancer cells.
Method: Pancreatic cancer cells were stimulated with VEGF165 for 1 or 2 h. The oxygen consumption rates (OCR) and extracellular acidification rates (ECAR) were measured using the Seahorse XF96 Extracellular Flux Analyzer. Glycolytic enzymes were detected by quantitative real-time PCR. Neuropilin 1 (NRP1) was silenced by shRNA in order to investigate its role in VEGF-induced glycolysis. Immunohistochemistry (IHC) was performed to identify the correlation among VEGF, NRP1 and hypoxia inducible factor 1α (HIF1α) in pancreatic cancer tissues.
Results: VEGF stimulation led to a metabolic transition from mitochondrial oxidative phosphorylation to glycolysis in pancreatic cancer. HIF1α and NRP1 protein levels were both increased after VEGF stimulation. The down-regulation of NRP1 reduced glycolysis in pancreatic cancer cells. NRP1 and VEGF levels both correlated with HIF1α expression in pancreatic tumor tissues.
Conclusion: VEGF enhances glycolysis in pancreatic cancer via HIF1α up-regulation. NRP1 plays a key role in VEGF-induced glycolysis.
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Cite this article as:
S. Shi, J. Xu, B. Zhang, S. Ji, W. Xu, J. Liu, K. Jin, D. Liang, C. Liang, L. Liu, C. Liu, Y. Qin, X. Yu , VEGF Promotes Glycolysis in Pancreatic Cancer via HIF1α Up-Regulation, Current Molecular Medicine 2016; 16 (4) . https://dx.doi.org/10.2174/1566524016666160316153623
DOI https://dx.doi.org/10.2174/1566524016666160316153623 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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