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胞质5'-核苷酸酶cN-II降低了人乳腺癌细胞对葡萄糖剥夺的适应性。

The cytosolic 5'-nucleotidase cN-II lowers the adaptability to glucose deprivation in human breast cancer cells.

作者信息

Bricard Gabriel, Cadassou Octavia, Cassagnes Laure-Estelle, Cros-Perrial Emeline, Payen-Gay Léa, Puy Jean-Yves, Lefebvre-Tournier Isabelle, Tozzi Maria Grazia, Dumontet Charles, Jordheim Lars Petter

机构信息

Université De Lyon, Université Claude Bernard Lyon 1, INSERM 1052, CNRS 5286, Centre Léon Bérard, Centre de Recherche en Cancérologie de Lyon, Lyon, France.

Biochemistry Laboratory of Lyon Sud, Hospices Civils de Lyon, Lyon, France.

出版信息

Oncotarget. 2017 Jun 27;8(40):67380-67393. doi: 10.18632/oncotarget.18653. eCollection 2017 Sep 15.

DOI:10.18632/oncotarget.18653
PMID:28978040
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5620180/
Abstract

The cytosolic 5'-nucleotidase cN-II is a highly conserved enzyme implicated in nucleotide metabolism. Based on recent observations suggesting additional roles not directly associated to its enzymatic activity, we studied human cancer cell models with basal or decreased cN-II expression. We developed cancer cells with stable inhibition of cN-II expression by transfection of shRNA-coding plasmids, and studied their biology. We show that human breast cancer cells MDA-MB-231 with decreased cN-II expression better adapt to the disappearance of glucose in growth medium under normoxic conditions than cells with a baseline expression level. This is associated with enhanced growth and a lower content of ROS in cells cultivated in absence of glucose due to more efficient mechanisms of elimination of ROS. Conversely, cells with low cN-II expression are more sensitive to glucose deprivation in hypoxic conditions. Overall, our results show that cN-II regulates the cellular response to glucose deprivation through a mechanism related to ROS metabolism and defence.

摘要

胞质5'-核苷酸酶cN-II是一种与核苷酸代谢相关的高度保守的酶。基于最近的观察结果表明其存在与酶活性不直接相关的其他作用，我们研究了cN-II表达基础水平或降低的人类癌细胞模型。我们通过转染编码短发夹RNA的质粒来稳定抑制cN-II的表达，从而构建癌细胞，并研究它们的生物学特性。我们发现，与基线表达水平的细胞相比，cN-II表达降低的人乳腺癌细胞MDA-MB-231在常氧条件下能更好地适应生长培养基中葡萄糖的消失。这与在无葡萄糖培养的细胞中生长增强以及由于更有效的活性氧消除机制而使活性氧含量降低有关。相反，cN-II表达低的细胞在缺氧条件下对葡萄糖剥夺更敏感。总体而言，我们的结果表明，cN-II通过与活性氧代谢和防御相关的机制调节细胞对葡萄糖剥夺的反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2be/5620180/35cc747df59e/oncotarget-08-67380-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2be/5620180/cdc57b6f5859/oncotarget-08-67380-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2be/5620180/d9f0f43fe265/oncotarget-08-67380-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2be/5620180/6c2a02aba291/oncotarget-08-67380-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2be/5620180/8de0d2151dcc/oncotarget-08-67380-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2be/5620180/b3aa4c1f547d/oncotarget-08-67380-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2be/5620180/31694ccf51de/oncotarget-08-67380-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2be/5620180/94fbe5925d14/oncotarget-08-67380-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2be/5620180/35cc747df59e/oncotarget-08-67380-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2be/5620180/cdc57b6f5859/oncotarget-08-67380-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2be/5620180/d9f0f43fe265/oncotarget-08-67380-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2be/5620180/6c2a02aba291/oncotarget-08-67380-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2be/5620180/8de0d2151dcc/oncotarget-08-67380-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2be/5620180/b3aa4c1f547d/oncotarget-08-67380-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2be/5620180/31694ccf51de/oncotarget-08-67380-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2be/5620180/94fbe5925d14/oncotarget-08-67380-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2be/5620180/35cc747df59e/oncotarget-08-67380-g008.jpg

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