缺氧调节胰腺癌的膜力学。

IF 2.9 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Prema Kumari Agarwala, Shobhna Kapoor
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引用次数: 0

摘要

侵袭性癌细胞如胰腺细胞表现出增强的转移表型,涉及细胞迁移和侵袭。细胞膜变形是细胞运动的一个关键过程。这暗示了在癌症进展过程中脂质代谢的改变和膜特性的调节以及相关功能之间的联系。胰腺癌侵袭性的关键因素之一是存在最高比例的缺氧,这进一步增加了脂质代谢重编程。本研究结合细胞生物学、显微镜和光谱学研究了缺氧诱导的脂质组改变对控制细胞运动的膜特性的后续影响。我们的研究结果表明,缺氧以细胞系依赖的方式诱导不同的脂质组特征,这反过来又差异地调节细胞膜刚度。细胞刚度与其他膜特性和肌动蛋白细胞骨架的相关性显示出随机相关性,表明缺氧应激明显调节控制细胞功能的特定膜特性,应参考胰腺癌有效治疗方法的发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hypoxia Modulates Membrane Mechanics in Pancreatic Cancer.

Aggressive cancer cells such as pancreatic cells exhibit an enhanced metastatic phenotype that involves cell migration and invasion. Cellular membrane deformation is a key process implicit in cell movement. This implicates a link between altered lipid metabolism during cancer progression and modulated membrane properties and hence associated functions. One of the key factors underlying the aggressiveness of pancreatic cancer is the presence of the highest percentage of hypoxia, which further adds to the lipid metabolic reprogramming. The subsequent effect of hypoxia-induced lipidome changes on membrane properties governing cell movement was investigated in this work using a combination of cell biology, microscopy, and spectroscopy. Our findings revealed that hypoxia induces distinct lipidome signatures in a cell-line-dependent fashion, which in turn differentially modulates the cell membrane stiffness. The correlation of cell stiffness with other membrane properties and the actin cytoskeleton shows a random correlation indicating that hypoxic stress distinctly regulates specific membrane attributes governing cellular functioning and should be consulted for the development of effective treatments for pancreatic cancer.

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来源期刊
Journal of Membrane Biology
Journal of Membrane Biology 生物-生化与分子生物学
CiteScore
4.80
自引率
4.20%
发文量
63
审稿时长
6-12 weeks
期刊介绍: The Journal of Membrane Biology is dedicated to publishing high-quality science related to membrane biology, biochemistry and biophysics. In particular, we welcome work that uses modern experimental or computational methods including but not limited to those with microscopy, diffraction, NMR, computer simulations, or biochemistry aimed at membrane associated or membrane embedded proteins or model membrane systems. These methods might be applied to study topics like membrane protein structure and function, membrane mediated or controlled signaling mechanisms, cell-cell communication via gap junctions, the behavior of proteins and lipids based on monolayer or bilayer systems, or genetic and regulatory mechanisms controlling membrane function. Research articles, short communications and reviews are all welcome. We also encourage authors to consider publishing ''negative'' results where experiments or simulations were well performed, but resulted in unusual or unexpected outcomes without obvious explanations. While we welcome connections to clinical studies, submissions that are primarily clinical in nature or that fail to make connections to the basic science issues of membrane structure, chemistry and function, are not appropriate for the journal. In a similar way, studies that are primarily descriptive and narratives of assays in a clinical or population study are best published in other journals. If you are not certain, it is entirely appropriate to write to us to inquire if your study is a good fit for the journal.
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