Complexities of lysophospholipid signalling in glioblastoma

Wayne Ng; Alice Pébay; Katharine Drummond; Antony Burgess; Andrew H Kaye; Andrew Morokoff

doi:10.1016/j.jocn.2014.02.013

Complexities of lysophospholipid signalling in glioblastoma

J Clin Neurosci. 2014 Jun;21(6):893-8. doi: 10.1016/j.jocn.2014.02.013. Epub 2014 Apr 18.

Authors

Wayne Ng¹, Alice Pébay², Katharine Drummond¹, Antony Burgess³, Andrew H Kaye⁴, Andrew Morokoff⁵

Affiliations

¹ University of Melbourne, Parkville, VIC, Australia; Department of Surgery, Royal Melbourne Hospital, Grattan Street, Parkville, VIC 3050, Australia; Department of Neurosurgery, Royal Melbourne Hospital, Parkville, VIC, Australia; Melbourne Brain Centre at Royal Melbourne Hospital, Parkville, VIC, Australia.
² University of Melbourne, Parkville, VIC, Australia; Centre for Eye Research Australia, Royal Victorian Eye and Ear Hospital, East Melbourne, VIC, Australia.
³ University of Melbourne, Parkville, VIC, Australia; Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia.
⁴ University of Melbourne, Parkville, VIC, Australia; Department of Surgery, Royal Melbourne Hospital, Grattan Street, Parkville, VIC 3050, Australia; Department of Neurosurgery, Royal Melbourne Hospital, Parkville, VIC, Australia.
⁵ University of Melbourne, Parkville, VIC, Australia; Department of Surgery, Royal Melbourne Hospital, Grattan Street, Parkville, VIC 3050, Australia; Department of Neurosurgery, Royal Melbourne Hospital, Parkville, VIC, Australia. Electronic address: [email protected].

PMID: 24746442
DOI: 10.1016/j.jocn.2014.02.013

Abstract

Glioblastoma multiforme (GBM) is the most malignant brain tumour and continues to have a very poor median survival of 12-16 months despite current best therapies. These aggressive tumours always recur after treatment and are defined by their ability to diffusely infiltrate and invade normal brain parenchyma. Autotaxin is overexpressed in GBM, and is a potent chemotactic enzyme that produces lysophosphatidic acid. Lysophospholipid (LPL) signalling is known to increase invasion of solid tumours and is also dysregulated in GBM. The LPL pathway has been shown to interact with known cancer-related signalling pathways, including those for epidermal growth factor and yes-associated protein, which are also dysregulated in GBM. The interactions between these pathways provide insights into the complexities of cancer signalling and suggest potential novel targets for GBM.

Keywords: Autotaxin; Glioblastoma multiforme; Lysophosphatidic acid.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

Animals
Brain Neoplasms / diagnosis
Brain Neoplasms / metabolism*
Cell Movement / physiology
Glioblastoma / diagnosis
Glioblastoma / metabolism*
Humans
Lysophospholipids / metabolism*
Neovascularization, Pathologic / diagnosis
Neovascularization, Pathologic / metabolism
Signal Transduction / physiology*

Substances

Lysophospholipids
lysophosphatidic acid