ArticleNeoplasia (New York, N.Y.)2006
Mechanisms of indomethacin-induced alterations in the choline phospholipid metabolism of breast cancer cells.
Article in Neoplasia (New York, N.Y.), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Trial
- LDH-Indomethacin Nanoparticles Antitumoral Action: A Possible Coadjuvant Drug for Cancer Therapy.Molecules (Basel, Switzerland) · 2024Article
- Monoethanolamine-induced glucose deprivation promotes apoptosis through metabolic rewiring in prostate cancer.Theranostics · 2021Article
- Applications of high-resolution magic angle spinning MRS in biomedical studies II-Human diseases.NMR in biomedicine · 2017Review
- Interplay of choline metabolites and genes in patient-derived breast cancer xenografts.Breast cancer research : BCR · 2014Article
- Identification of human disease genes from interactome network using graphlet interaction.PloS one · 2014Article
- Choline metabolism in malignant transformation.Nature reviews. Cancer · 2011Review
- Multimodal mass spectrometric imaging of small molecules reveals distinct spatio-molecular signatures in differentially metastatic breast tumor models.Cancer research · 2010Article
- Distinct choline metabolic profiles are associated with differences in gene expression for basal-like and luminal-like breast cancer xenograft models.BMC cancer · 2010Article
- Total choline at 1H-MRS and [18F]-fluoromethylcholine uptake at PET.Molecular imaging and biology · 2010Article
- Metabolic assessment of the action of targeted cancer therapeutics using magnetic resonance spectroscopy.British journal of cancer · 2010Review
- 17-allyamino-17-demethoxygeldanamycin treatment results in a magnetic resonance spectroscopy-detectable elevation in choline-containing metabolites associated with increased expression of choline transporter SLC44A1 and phospholipase A2.Breast cancer research : BCR · 2010Article
- Toward digital staining using imaging mass spectrometry and random forests.Journal of proteome research · 2009Article
- Lysophosphatidylcholine acyltransferase 1 (LPCAT1) overexpression in human colorectal cancer.Journal of molecular medicine (Berlin, Germany) · 2009Article
- Neoplasia: the second decade.Neoplasia (New York, N.Y.) · 2008Article
- Quantification of choline- and ethanolamine-containing metabolites in human prostate tissues using 1H HR-MAS total correlation spectroscopy.Magnetic resonance in medicine · 2008Article
- Anti-inflammatory agent indomethacin reduces invasion and alters metabolism in a human breast cancer cell line.Neoplasia (New York, N.Y.) · 2007Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Human mammary epithelial cells (HMECs) exhibit an increase in phosphocholine (PC) and total choline-containing compounds, as well as a switch from high glycerophosphocholine (GPC)/low PC to low GPC/high PC, with progression to malignant phenotype. The treatment of human breast cancer cells with a nonsteroidal anti-inflammatory agent, indomethacin, reverted the high PC/low GPC pattern to a low PC/high GPC pattern indicative of a less malignant phenotype, supported by decreased invasion. Here, we have characterized mechanisms underlying indomethacin-induced alterations in choline membrane metabolism in malignant breast cancer cells and nonmalignant HMECs labeled with [1,2-13C]choline using 1H and 13C magnetic resonance spectroscopy. Microarray gene expression analysis was performed to understand the molecular mechanisms underlying these changes. In breast cancer cells, indomethacin treatment activated phospholipases that, combined with an increased choline phospholipid biosynthesis, led to increased GPC and decreased PC levels. However, in nonmalignant HMECs, activation of the anabolic pathway alone was detected following indomethacin treatment. Following indomethacin treatment in breast cancer cells, several candidate genes, such as interleukin 8, NGFB, CSF2, RHOB, EDN1, and JUNB, were differentially expressed, which may have contributed to changes in choline metabolism through secondary effects or signaling cascades leading to changes in enzyme activity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.