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Role of Gremlin-1 in Cancer
Biomed Sci Letters 2018;24:285-291
Published online December 31, 2018;  https://doi.org/10.15616/BSL.2018.24.4.285
© 2018 The Korean Society For Biomedical Laboratory Sciences.

Sin-Aye Park†,*

Department of Biomedical Laboratory Science, College of Medical Sciences, Soonchunhyang University, Asan 31538, Korea
Correspondence to: *Professor.
Sin-Aye Park. Department of Biomedical Laboratory Science, College of Medical Sciences, Soonchunhyang University, Asan 31538, Korea.
Tel: +82-41-530-4990, Fax: +82-41-530-3085, e-mail: sappark@sch.ac.kr
Received October 22, 2018; Accepted December 4, 2018.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
 Abstract
Gremlin-1 (GREM1) has been defined as an antagonist of bone morphogenetic proteins (BMPs), particularly during embryonic development and tissue differentiation. However, recent studies have shown that GREM1 has BMPs-dependent or -independent functions in diverse human diseases. GREM1 plays a key role in the process of organ fibrosis, including lungs, kidneys, and so on. The GREM1-induced fibrosis typically promotes the development of other diseases, such as pulmonary hypertension, renal inflammation, and diabetic nephropathy. More recently, considerable evidence has been reported showing that GREM1 is involved in the promotion and/or progression of tumors in vitro and in vivo. It also performs an oncogenic role in the maintenance of cancer stem cells. Although GREM1 is known to function in a variety of diseases, here we focus on the role of GREM1 in cancer, and suggest GREM1 as a potential therapeutic target in certain types of cancer.
Keywords : Gremlin-1, Epithelial-mesenchymal transition, Fibrosis, Cancer, Angiogenesis