Journal
CELLS
Volume 10, Issue 4, Pages -Publisher
MDPI
DOI: 10.3390/cells10040939
Keywords
Autotaxin (ATX); lysophosphatidic acid (LPA); ATX-LPA axis; cancer
Categories
Funding
- National Natural Science Foundation of China [81972604, 31500619]
- Beijing Natural Science Foundation [7192102, 5172019]
- Open Fund from the Key Laboratory of Cell Proliferation and Regulation Biology, Ministry of Education, China
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Autotaxin plays a crucial role in cancer development by promoting cell proliferation, migration, and survival through producing LPA, as well as increasing the expression of inflammation-related circuits that impact patients' prognosis. ATX is considered a potential therapeutic target for cancer, with a number of ATX inhibitors currently developed.
Autotaxin (ATX) is a secreted glycoprotein and functions as a key enzyme to produce extracellular lysophosphatidic acid (LPA). LPA interacts with at least six G protein-coupled receptors, LPAR1-6, on the cell membrane to activate various signal transduction pathways through distinct G proteins, such as Gi/0, G12/13, Gq/11, and Gs. The ATX-LPA axis plays an important role in physiological and pathological processes, including embryogenesis, obesity, and inflammation. ATX is one of the top 40 most unregulated genes in metastatic cancer, and the ATX-LPA axis is involved in the development of different types of cancers, such as colorectal cancer, ovarian cancer, breast cancer, and glioblastoma. ATX expression is under multifaceted controls at the transcription, post-transcription, and secretion levels. ATX and LPA in the tumor microenvironment not only promote cell proliferation, migration, and survival, but also increase the expression of inflammation-related circuits, which results in poor outcomes for patients with cancer. Currently, ATX is regarded as a potential cancer therapeutic target, and an increasing number of ATX inhibitors have been developed. In this review, we focus on the mechanism of ATX expression regulation and the functions of ATX in cancer development.
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