Complexities of lysophospholipid signalling in glioblastoma

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.