Special Issue "Lysophosphatidic Acid Signalling in Cancer"
A special issue of Cancers (ISSN 2072-6694).
Deadline for manuscript submissions: 15 August 2019
Prof. Dr. David Brindley
Signal Transduction Research Group, Cancer Research Institute of Northern Alberta, Department of Biochemistry, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB T6G 2S2, Canada
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Interests: breast cancer; metastasis; inflammation; chemo-resistance; radiation-induced fibrosis; autotaxin; lysophosphatidic acid; lipid phosphate phosphatases
It is now just over 25 years since the separate discoveries of autotaxin (ATX) and the role of lysophosphatidic acid (lysophosphatidate, LPA) as a signaling molecule. The identification of six G-protein-coupled receptors for LPA was a major breakthrough in understanding the role of extracellular LPA in cell signaling. The work on ATX and LPA signaling came together about 18 years ago after ATX was identified as the enzyme that produces the majority of extracellular LPA. The other major component of the LPA signaling system is its termination through the degradation of extracellular LPA by a family of three lipid phosphate phosphatases (LPP1–3).
This Special Issue of Cancers will focus specifically on the role of LPA signaling in cancers and their treatments. The net effects of LPA signaling in cancers are increased in various tumors through increased ATX secretion coupled with a decrease in the expression of LPP1 and LPP3. LPA signaling is now being recognized as a central mediator of the progression of chronic inflammation in the tumor microenvironment and a component of several of the hallmarks of cancer. LPA promotes tumor growth and metastasis, and facilitates immune evasion. The role of LPA as a pro-survival signal also explains why LPA decreases the efficacy of several chemotherapeutic agents and also protects cancer cells from cell death caused by ionizing radiation.
There are now a variety of therapeutic agents which inhibit LPA synthesis by ATX, LPA signaling through its receptors, and increase LPA degradation. So far, these have not been used to decrease the adverse effects of LPA signaling in the management of cancer patients. We are now at the exciting point of being able to target LPA signaling as a novel paradigm for improving existing cancer treatments.
Prof. Dr. David Brindley
Manuscript Submission Information
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