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本文引用的文献

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Metabolic rewiring of pancreatic ductal adenocarcinoma: New routes to follow within the maze.胰腺导管腺癌的代谢重编程：迷宫中可供追寻的新路径。
Int J Cancer. 2016 Feb 15;138(4):787-96. doi: 10.1002/ijc.29501. Epub 2015 Mar 18.
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Pancreatic cancer: Disrupted lipid metabolic pathways in PDAC identified.
Nat Rev Gastroenterol Hepatol. 2015 Apr;12(4):188. doi: 10.1038/nrgastro.2015.32. Epub 2015 Feb 24.
3
Cholesterol uptake disruption, in association with chemotherapy, is a promising combined metabolic therapy for pancreatic adenocarcinoma.胆固醇摄取阻断联合化疗是一种有前景的胰腺癌联合代谢疗法。
Proc Natl Acad Sci U S A. 2015 Feb 24;112(8):2473-8. doi: 10.1073/pnas.1421601112. Epub 2015 Feb 9.
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Association between cholesterol intake and pancreatic cancer risk: evidence from a meta-analysis.胆固醇摄入量与胰腺癌风险之间的关联：一项荟萃分析的证据。
Sci Rep. 2015 Feb 4;5:8243. doi: 10.1038/srep08243.
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Famine versus feast: understanding the metabolism of tumors in vivo.饥荒与盛宴：理解体内肿瘤的代谢
Trends Biochem Sci. 2015 Mar;40(3):130-40. doi: 10.1016/j.tibs.2015.01.004. Epub 2015 Jan 29.
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Pancreatic adenocarcinoma.胰腺腺癌
N Engl J Med. 2014 Sep 11;371(11):1039-49. doi: 10.1056/NEJMra1404198.
7
O-GlcNAcylation regulates cancer metabolism and survival stress signaling via regulation of the HIF-1 pathway.O-GlcNAcylation 通过调节 HIF-1 通路来调节癌症代谢和生存应激信号。
Mol Cell. 2014 Jun 5;54(5):820-31. doi: 10.1016/j.molcel.2014.04.026. Epub 2014 May 22.
8
Lipogenesis and lipolysis: the pathways exploited by the cancer cells to acquire fatty acids.脂肪生成和脂肪分解：癌细胞获取脂肪酸所利用的途径。
Prog Lipid Res. 2013 Oct;52(4):585-9. doi: 10.1016/j.plipres.2013.08.005. Epub 2013 Aug 31.
9
Strengthened glycolysis under hypoxia supports tumor symbiosis and hexosamine biosynthesis in pancreatic adenocarcinoma.缺氧条件下增强的糖酵解支持胰腺腺癌中的肿瘤共生和己糖胺生物合成。
Proc Natl Acad Sci U S A. 2013 Mar 5;110(10):3919-24. doi: 10.1073/pnas.1219555110. Epub 2013 Feb 13.
10
Phosphofructokinase 1 glycosylation regulates cell growth and metabolism.磷酸果糖激酶 1 糖基化调节细胞生长和代谢。
Science. 2012 Aug 24;337(6097):975-80. doi: 10.1126/science.1222278.

低密度脂蛋白受体：为胰腺肿瘤细胞提供营养的一条开放途径。

LDL Receptor: An open route to feed pancreatic tumor cells.

作者信息

Vasseur Sophie, Guillaumond Fabienne

机构信息

INSERM, U1068, Centre de Recherche en Cancérologie de Marseille, Marseille, France; Institut Paoli-Calmettes, Marseille, France; CNRS, UMR7258, Marseille, France; Université Aix-Marseille, Marseille, France.

出版信息

Mol Cell Oncol. 2015 May 7;3(1):e1033586. doi: 10.1080/23723556.2015.1033586. eCollection 2016 Jan.

DOI:10.1080/23723556.2015.1033586
PMID:27308549
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4845189/
Abstract

The role of altered lipid metabolism in pancreatic ductal adenocarcinoma (PDAC) is poorly appreciated. We recently identified the lipid signature of PDAC and revealed low-density lipoprotein receptor (Ldlr) as a metabolic driver of this disease. Here, we comment our findings that disruption of Ldlr leads to intratumoral cholesterol imbalance and improves chemotherapy efficiency.

摘要

脂质代谢改变在胰腺导管腺癌（PDAC）中的作用尚未得到充分认识。我们最近确定了PDAC的脂质特征，并揭示低密度脂蛋白受体（Ldlr）是这种疾病的代谢驱动因素。在此，我们对我们的研究结果进行评论，即Ldlr的破坏会导致肿瘤内胆固醇失衡并提高化疗效率。