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Role of Human Galectins in Inflammation and Cancers Associated with Endometriosis.

Authors :
Hisrich BV
Young RB
Sansone AM
Bowens Z
Green LJ
Lessey BA
Blenda AV
Source :
Biomolecules [Biomolecules] 2020 Feb 04; Vol. 10 (2). Date of Electronic Publication: 2020 Feb 04.
Publication Year :
2020

Abstract

Galectins are a family of β-galactoside-binding proteins that contribute to multiple cellular functions, including immune surveillance and apoptosis. Human galectins are also important regulators of inflammation, making them a research target for various inflammatory diseases and tumorigenesis associated with pro-inflammatory conditions. This review focuses on the involvement of human galectins in modulation of inflammation and in the pathophysiology of endometriosis and endometriosis-associated neoplasms. Endometriosis is a chronic inflammatory disease with unknown etiology. Galectins -1, -3 and -9 were found to be overexpressed in ectopic and eutopic endometrium of females with endometriosis compared to those without endometriosis. These findings suggest galectins' role in the progression on endometriotic lesions and their potential use as diagnostic biomarkers and/or targets for therapeutic approaches. Galectins -1, -3, and -9 have also been implicated in the development of endometriosis-associated neoplasms. Furthermore, galectin-3 has been shown to interact with KRAS protein and contribute to cellular growth, proliferation, inflammation, and the uptake of nutrients in endometriotic lesions and may be involved in the maintenance and propagation of endometriosis. These galectins have been shown to be upregulated in certain forms of cervical, ovarian, endometrial, and colon cancer associated with endometriosis and have become a potential target for anti-cancer therapies.<br />Competing Interests: The authors declare no conflict of interest.

Details

Language :
English
ISSN :
2218-273X
Volume :
10
Issue :
2
Database :
MEDLINE
Journal :
Biomolecules
Publication Type :
Academic Journal
Accession number :
32033052
Full Text :
https://doi.org/10.3390/biom10020230