Exposure of human breast cancer cells to the anti-inflammatory agent indomethacin alters choline phospholipid metabolites and Nm23 expression

Research output: Contribution to journalArticle

Abstract

We previously observed that changes in choline phospholipids of two malignant human mammary epithelial cells (HMECs) following treatment with a high dose of the cyclooxygenase (COX) inhibitor, indomethacin, mimicked changes following transfection with a metastasis suppressor gene, nm23. The similarity between response to indomethacin and nm23transfection led us to 1) expand our 1H NMR spectroscopy study of indomethacin treatment by determining the response at two doses for two nonmalignant and three malignant HMECs, 2) investigate COX-1 and COX-2 levels in HMECs and their relationship with choline phosholipid metabolites, and 3) determine changes in Nm23 expression following treatment with indomethacin. All HMECs exhibited a significant change in choline phospholipids following treatment with 300 μM indomethacin. At the lower dose of 50 μM, only nonmalignant HMECs and the estrogen-dependent malignant cell line, MCF-7, responded. COX-1 levels were significantly higher in malignant HMECs than in nonmalignant HMECs. A significant increase in Nm23 expression following 300 μM indomethacin was detected in MCF- 12A and MCF-7 cells but not in MDA-MB-231 and MDA-MB-435 cells. These results suggest that COX-1 expression and its inhibition play a role in the choline phospholipid metabolism of HMECs, and the effect of indomethacin on HMECs may be mediated, in part, through upregulation of nm23.

Original languageEnglish (US)
Pages (from-to)409-416
Number of pages8
JournalNeoplasia
Volume4
Issue number5
DOIs
StatePublished - Sep 2002

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Choline
Indomethacin
Phospholipids
Breast
Anti-Inflammatory Agents
Epithelial Cells
Breast Neoplasms
Cyclooxygenase 1
Cyclooxygenase Inhibitors
MCF-7 Cells
Cyclooxygenase 2
Tumor Suppressor Genes
Transfection
Estrogens
Up-Regulation
Magnetic Resonance Spectroscopy
Cell Line

Keywords

  • Anti-inflammatory agent
  • Breast cancer cells
  • Choline phospholipid metabolites
  • Nm23 expression
  • NMR spectroscopy

ASJC Scopus subject areas

  • Cancer Research

Cite this

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title = "Exposure of human breast cancer cells to the anti-inflammatory agent indomethacin alters choline phospholipid metabolites and Nm23 expression",
abstract = "We previously observed that changes in choline phospholipids of two malignant human mammary epithelial cells (HMECs) following treatment with a high dose of the cyclooxygenase (COX) inhibitor, indomethacin, mimicked changes following transfection with a metastasis suppressor gene, nm23. The similarity between response to indomethacin and nm23transfection led us to 1) expand our 1H NMR spectroscopy study of indomethacin treatment by determining the response at two doses for two nonmalignant and three malignant HMECs, 2) investigate COX-1 and COX-2 levels in HMECs and their relationship with choline phosholipid metabolites, and 3) determine changes in Nm23 expression following treatment with indomethacin. All HMECs exhibited a significant change in choline phospholipids following treatment with 300 μM indomethacin. At the lower dose of 50 μM, only nonmalignant HMECs and the estrogen-dependent malignant cell line, MCF-7, responded. COX-1 levels were significantly higher in malignant HMECs than in nonmalignant HMECs. A significant increase in Nm23 expression following 300 μM indomethacin was detected in MCF- 12A and MCF-7 cells but not in MDA-MB-231 and MDA-MB-435 cells. These results suggest that COX-1 expression and its inhibition play a role in the choline phospholipid metabolism of HMECs, and the effect of indomethacin on HMECs may be mediated, in part, through upregulation of nm23.",
keywords = "Anti-inflammatory agent, Breast cancer cells, Choline phospholipid metabolites, Nm23 expression, NMR spectroscopy",
author = "Kshama Natarajan and Noriko Mori and Dmitri Artemov and Bhujwalla, {Zaver M}",
year = "2002",
month = "9",
doi = "10.1038/sj.neo.7900252",
language = "English (US)",
volume = "4",
pages = "409--416",
journal = "Neoplasia",
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number = "5",

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T1 - Exposure of human breast cancer cells to the anti-inflammatory agent indomethacin alters choline phospholipid metabolites and Nm23 expression

AU - Natarajan, Kshama

AU - Mori, Noriko

AU - Artemov, Dmitri

AU - Bhujwalla, Zaver M

PY - 2002/9

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N2 - We previously observed that changes in choline phospholipids of two malignant human mammary epithelial cells (HMECs) following treatment with a high dose of the cyclooxygenase (COX) inhibitor, indomethacin, mimicked changes following transfection with a metastasis suppressor gene, nm23. The similarity between response to indomethacin and nm23transfection led us to 1) expand our 1H NMR spectroscopy study of indomethacin treatment by determining the response at two doses for two nonmalignant and three malignant HMECs, 2) investigate COX-1 and COX-2 levels in HMECs and their relationship with choline phosholipid metabolites, and 3) determine changes in Nm23 expression following treatment with indomethacin. All HMECs exhibited a significant change in choline phospholipids following treatment with 300 μM indomethacin. At the lower dose of 50 μM, only nonmalignant HMECs and the estrogen-dependent malignant cell line, MCF-7, responded. COX-1 levels were significantly higher in malignant HMECs than in nonmalignant HMECs. A significant increase in Nm23 expression following 300 μM indomethacin was detected in MCF- 12A and MCF-7 cells but not in MDA-MB-231 and MDA-MB-435 cells. These results suggest that COX-1 expression and its inhibition play a role in the choline phospholipid metabolism of HMECs, and the effect of indomethacin on HMECs may be mediated, in part, through upregulation of nm23.

AB - We previously observed that changes in choline phospholipids of two malignant human mammary epithelial cells (HMECs) following treatment with a high dose of the cyclooxygenase (COX) inhibitor, indomethacin, mimicked changes following transfection with a metastasis suppressor gene, nm23. The similarity between response to indomethacin and nm23transfection led us to 1) expand our 1H NMR spectroscopy study of indomethacin treatment by determining the response at two doses for two nonmalignant and three malignant HMECs, 2) investigate COX-1 and COX-2 levels in HMECs and their relationship with choline phosholipid metabolites, and 3) determine changes in Nm23 expression following treatment with indomethacin. All HMECs exhibited a significant change in choline phospholipids following treatment with 300 μM indomethacin. At the lower dose of 50 μM, only nonmalignant HMECs and the estrogen-dependent malignant cell line, MCF-7, responded. COX-1 levels were significantly higher in malignant HMECs than in nonmalignant HMECs. A significant increase in Nm23 expression following 300 μM indomethacin was detected in MCF- 12A and MCF-7 cells but not in MDA-MB-231 and MDA-MB-435 cells. These results suggest that COX-1 expression and its inhibition play a role in the choline phospholipid metabolism of HMECs, and the effect of indomethacin on HMECs may be mediated, in part, through upregulation of nm23.

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