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Autotaxin-Lysophosphatidic Acid: From Inflammation to Cancer Development
Joint Authors
Valdés-Rives, Silvia Anahi
González-Arenas, Aliesha
Source
Issue
Vol. 2017, Issue 2017 (31 Dec. 2017), pp.1-15, 15 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2017-12-21
Country of Publication
Egypt
No. of Pages
15
Main Subjects
Abstract EN
Lysophosphatidic acid (LPA) is a ubiquitous lysophospholipid and one of the main membrane-derived lipid signaling molecules.
LPA acts as an autocrine/paracrine messenger through at least six G protein-coupled receptors (GPCRs), known as LPA1–6, to induce various cellular processes including wound healing, differentiation, proliferation, migration, and survival.
LPA receptors and autotaxin (ATX), a secreted phosphodiesterase that produces this phospholipid, are overexpressed in many cancers and impact several features of the disease, including cancer-related inflammation, development, and progression.
Many ongoing studies aim to understand ATX-LPA axis signaling in cancer and its potential as a therapeutic target.
In this review, we discuss the evidence linking LPA signaling to cancer-related inflammation and its impact on cancer progression.
American Psychological Association (APA)
Valdés-Rives, Silvia Anahi& González-Arenas, Aliesha. 2017. Autotaxin-Lysophosphatidic Acid: From Inflammation to Cancer Development. Mediators of Inflammation،Vol. 2017, no. 2017, pp.1-15.
https://search.emarefa.net/detail/BIM-1188809
Modern Language Association (MLA)
Valdés-Rives, Silvia Anahi& González-Arenas, Aliesha. Autotaxin-Lysophosphatidic Acid: From Inflammation to Cancer Development. Mediators of Inflammation No. 2017 (2017), pp.1-15.
https://search.emarefa.net/detail/BIM-1188809
American Medical Association (AMA)
Valdés-Rives, Silvia Anahi& González-Arenas, Aliesha. Autotaxin-Lysophosphatidic Acid: From Inflammation to Cancer Development. Mediators of Inflammation. 2017. Vol. 2017, no. 2017, pp.1-15.
https://search.emarefa.net/detail/BIM-1188809
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1188809