Format

Send to

Choose Destination
NMR Biomed. 2018 Aug;31(8):e3936. doi: 10.1002/nbm.3936. Epub 2018 Jun 21.

Molecular causes of elevated phosphoethanolamine in breast and pancreatic cancer cells.

Author information

1
Division of Cancer Imaging Research, The Russell H Morgan Department of Radiology and Radiological Science, The Johns Hopkins University, School of Medicine, Baltimore, MD, USA.
2
Centre of Image Sciences/High Field MR Research Group, Radiology, University Medical Centre Utrecht, Utrecht, the Netherlands.
3
Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University, School of Medicine, Baltimore, MD, USA.
4
Department of Radiation Oncology and Molecular Radiation Sciences, The Johns Hopkins University, School of Medicine, Baltimore, MD, USA.

Abstract

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.

KEYWORDS:

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

PMID:
29928787
PMCID:
PMC6118328
[Available on 2019-08-01]
DOI:
10.1002/nbm.3936
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wiley
Loading ...
Support Center