Special Issue "Lysophosphatidic Acid Signalling in Cancer"

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: 15 August 2019

Special Issue Editor

Guest Editor
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
Website | E-Mail
Interests: breast cancer; metastasis; inflammation; chemo-resistance; radiation-induced fibrosis; autotaxin; lysophosphatidic acid; lipid phosphate phosphatases

Special Issue Information

Dear Colleagues,

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
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers (1 paper)

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Open AccessArticle Challenges and Inconsistencies in Using Lysophosphatidic Acid as a Biomarker for Ovarian Cancer
Cancers 2019, 11(4), 520; https://doi.org/10.3390/cancers11040520
Received: 11 March 2019 / Revised: 27 March 2019 / Accepted: 9 April 2019 / Published: 11 April 2019
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Increased detection of plasma lysophosphatidic acid (LPA) has been proposed as a potential diagnostic biomarker in ovarian cancer, but inconsistency exists in these reports. It has been shown that LPA can undergo an artificial increase during sample processing and analysis, which has not [...] Read more.
Increased detection of plasma lysophosphatidic acid (LPA) has been proposed as a potential diagnostic biomarker in ovarian cancer, but inconsistency exists in these reports. It has been shown that LPA can undergo an artificial increase during sample processing and analysis, which has not been accounted for in ovarian cancer research. The aim of this study is to provide a potential explanation about how the artificial increase in LPA may have interfered with previous LPA analysis in ovarian cancer research. Using an established LC-MS method, we measured LPA and other lysophospholipid levels in plasma obtained from three cohorts of patients: non-cancer controls, patients with benign ovarian tumors, and those with ovarian cancer. We did not find the LPA level to be higher in cancer samples. To understand this inconsistency, we observed that LPA content changed more significantly than other lysophospholipids as a function of plasma storage time while frozen. Additionally, only LPA was found to be adversely impacted by incubation time depending on the Ethylenediaminetetraacetic acid (EDTA) concentration used during blood drawing. We also show that the inhibition of autotaxin effectively prevented artificial LPA generation during incubation at room temperature. Our data suggests that the artificial changes in LPA content may contribute to the discrepancies reported in literature. Any future studies planning to measure plasma LPA should carefully design the study protocol to consider these confounding factors. Full article
(This article belongs to the Special Issue Lysophosphatidic Acid Signalling in Cancer)
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