Breast cancer cells that preferentially metastasize to lung or bone are more glycolytic, synthesize serine at greater rates, and consume less ATP and NADPH than parent MDA-MB-231 cells

糖酵解 氧化磷酸化 生物化学 厌氧糖酵解 谷氨酰胺 细胞培养 线粒体 化学 合成代谢 生物 新陈代谢 氨基酸 遗传学
作者
Mika B. Jekabsons,Mollie Merrell,Anna G. Skubiz,Noah Thornton,Sandra Milasta,Douglas R. Green,Taosheng Chen,Yan‐Hong Wang,Bharathi Avula,Ikhlas A. Khan,Yu‐Dong Zhou
出处
期刊:Cancer and Metabolism [BioMed Central]
卷期号:11 (1) 被引量:9
标识
DOI:10.1186/s40170-023-00303-5
摘要

Gene expression signatures associated with breast cancer metastases suggest that metabolic re-wiring is important for metastatic growth in lungs, bones, and other organs. However, since pathway fluxes depend on additional factors such as ATP demand, allosteric effects, and post-translational modification, flux analysis is necessary to conclusively establish phenotypes. In this study, the metabolic phenotypes of breast cancer cell lines with low (T47D) or high (MDA-MB-231) metastatic potential, as well as lung (LM)- and bone (BoM)-homing lines derived from MDA-MB-231 cells, were assessed by 13C metabolite labeling from [1,2-13C] glucose or [5-13C] glutamine and the rates of nutrient and oxygen consumption and lactate production. MDA-MB-231 and T47D cells produced 55 and 63%, respectively, of ATP from oxidative phosphorylation, whereas LM and BoM cells were more glycolytic, deriving only 20-25% of their ATP from mitochondria. ATP demand by BoM and LM cells was approximately half the rate of the parent cells. Of the anabolic fluxes assessed, nucleotide synthesis was the major ATP consumer for all cell lines. Glycolytic NADH production by LM cells exceeded the rate at which it could be oxidized by mitochondria, suggesting that the malate-aspartate shuttle was not involved in re-oxidation of these reducing equivalents. Serine synthesis was undetectable in MDA-MB-231 cells, whereas 3-5% of glucose was shunted to serine by LM and BoM lines. Proliferation rates of T47D, BoM, and LM lines tightly correlated with their respiration-normalized NADPH production rates. In contrast, MDA-MB-231 cells produced NADPH and GSH at higher rates, suggesting this line is more oxidatively stressed. Approximately half to two-thirds of NADPH produced by T47D, MDA-MB-231, and BoM cells was from the oxidative PPP, whereas the majority in LM cells was from the folate cycle. All four cell lines used the non-oxidative PPP to produce pentose phosphates, although this was most prominent for LM cells. Taken together, the metabolic phenotypes of LM and BoM lines differed from the parent line and from each other, supporting the metabolic re-wiring hypothesis as a feature of metastasis to lung and bone.

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
Orange的应助被王童采纳,获得10
1秒前
翟林林完成签到,获得积分20
1秒前
一颗石头鱼的应助被A_DAY采纳,获得10
2秒前
wjy发布了新的文献求助10
2秒前
汉堡包的应助被Cai采纳,获得10
3秒前
molihuakai的应助被jy采纳,获得10
6秒前
7秒前
7秒前
7秒前
7秒前
元柏完成签到 ,获得积分10
8秒前
8秒前
大模型的应助被摄青梦境采纳,获得30
8秒前
9秒前
hua完成签到,获得积分10
9秒前
10秒前
10秒前
王童完成签到,获得积分10
10秒前
如梦发布了新的文献求助10
11秒前
Owen的应助被积极问晴采纳,获得10
11秒前
11秒前
共享精神的应助被Jiuanpy采纳,获得10
11秒前
xiaozhao发布了新的文献求助10
12秒前
科研通AI6.4的应助被wjy采纳,获得10
12秒前
RON发布了新的文献求助10
13秒前
王童发布了新的文献求助10
14秒前
14秒前
zc发布了新的文献求助10
14秒前
煜宁HY发布了新的文献求助10
16秒前
儒偿所愿发布了新的文献求助10
16秒前
研友_8K2QJZ完成签到,获得积分10
17秒前
hxy给hxy的求助进行了留言
17秒前
一叶不知秋完成签到,获得积分10
18秒前
jessie完成签到,获得积分10
19秒前
19秒前
小二郎的应助被罗门采纳,获得10
20秒前
20秒前
火星上火发布了新的文献求助30
20秒前
小马甲的应助被lisheng采纳,获得10
20秒前
科研小啪菜完成签到,获得积分10
21秒前
高分求助中
(应助此贴封号)通过应助OA文献获取积分 10000
Rosenblum, Global Change Biology 800
Computational Chemical Reaction Engineering: Modeling, Simulation, and Design with MATLAB 600
Organizational Behavior 510
Management and the Arts 510
Production Logging: Theoretical and Interpretive Elements 400
CLSI C56QG Examples of Hemolyzed, Icteric, and Lipemic/Turbid Samples Quick Guide 400
热门求助领域 (近24小时)
化学 材料科学 医学 生物 计算机科学 工程类 纳米技术 内科学 物理 有机化学 化学工程 生物化学 复合材料 光电子学 细胞生物学 心理学 量子力学 催化作用 物理化学 电极
热门帖子
关注 科研通微信公众号,转发送积分 7817850
求助须知:如何正确求助?哪些是违规求助? 9346252
关于积分的说明 20534940
捐赠科研通 7410402
什么是DOI,文献DOI怎么找? 3331819
关于科研通互助平台的介绍 2478149
邀请新用户注册赠送积分活动 2351579