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Author Notes:

Correspondence to C. Chris Yun, Division of Digestive Diseases, Department of Medicine, Emory University School of Medicine, Whitehead Research Bldg. Room 201, 615 Michael Street, Atlanta, GA 30322, USA; ccyun@emory.edu; Tel.: +1-404-712-2865

The author declares no conflict of interest.

Subjects:

Research Funding:

This work was supported by NIH grants R01DK071597, R01DK116799 and the VA Merit award I01BX002540.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Oncology
  • lysophosphatidic acid
  • colorectal cancer
  • inflammation
  • intestine
  • PROTEIN-COUPLED RECEPTOR
  • INTESTINAL EPITHELIAL-CELLS
  • HUMAN-COLON-CARCINOMA
  • NA+/H+ EXCHANGER 3
  • ULCERATIVE-COLITIS
  • LPA RECEPTORS
  • GROWTH-FACTOR
  • MEDIATED PHOSPHORYLATION
  • ABERRANT EXPRESSION
  • LYSOPHOSPHOLIPASE-D

Lysophosphatidic Acid and Autotaxin-associated Effects on the Initiation and Progression of Colorectal Cancer

Tools:

Journal Title:

Cancers

Volume:

Volume 11, Number 7

Publisher:

Type of Work:

Article | Final Publisher PDF

Abstract:

The intestinal epithelium interacts dynamically with the immune system to maintain its barrier function to protect the host, while performing the physiological roles in absorption of nutrients, electrolytes, water and minerals. The importance of lysophosphatidic acid (LPA) and its receptors in the gut has been progressively appreciated. LPA signaling modulates cell proliferation, invasion, adhesion, angiogenesis, and survival that can promote cancer growth and metastasis. These effects are equally important for the maintenance of the epithelial barrier in the gut, which forms the first line of defense against the milieu of potentially pathogenic stimuli. This review focuses on the LPA-mediated signaling that potentially contributes to inflammation and tumor formation in the gastrointestinal tract.

Copyright information:

© 2019 by the author. Licensee MDPI, Basel, Switzerland.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).
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