Molecular causes of elevated phosphoethanolamine in breast and pancreatic cancer cells

Tariq Shah, Balaji Krishnamachary, Flonne Wildes, Jannie P. Wijnen, Kristine Glunde, Zaver M. Bhujwalla

Research output: Contribution to journalArticlepeer-review

6 Scopus citations


Elevated phosphoethanolamine (PE) is frequently observed in MRS studies of human cancers and xenografts. The role of PE in cell survival and the molecular causes underlying this increase are, however, relatively underexplored. In this study, we investigated the roles of ethanolamine kinases (Etnk-1 and 2) and choline kinases (Chk-α and β) in contributing to increased PE in human breast and pancreatic cancer cells. We investigated the effect of silencing Etnk-1 and Etnk-2 on cell viability as a potential therapeutic strategy. Both breast and pancreatic cancer cells showed higher PE compared with their nonmalignant counterparts. We identified Etnk-1 as a major cause of the elevated PE levels in these cancer cells, with little or no contribution from Chk-α, Chk-β, or Etnk-2. The increase of PE observed in pancreatic cancer cells in culture was replicated in the corresponding tumor xenografts. Downregulation of Etnk-1 with siRNA resulted in cell cytotoxicity that correlated with PE levels in breast and pancreatic cancer cells. Etnk-1 may provide a potential therapeutic target in breast and pancreatic cancers.

Original languageEnglish (US)
Article numbere3936
JournalNMR in biomedicine
Issue number8
StatePublished - Aug 2018


  • MRS
  • breast cancer
  • choline kinase
  • ethanolamine kinase
  • metabolism
  • pancreatic cancer

ASJC Scopus subject areas

  • Molecular Medicine
  • Radiology Nuclear Medicine and imaging
  • Spectroscopy


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