The Nm23-H1 metastasis suppressor as a translational target |
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| Authors: | Jean-Claude Marshall Joshua Collins Natascia Marino Patricia Steeg |
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| Affiliation: | 1. Translational Research Group, the Heart Research Institute, Sydney 2042, Australia;2. University of Sydney, Sydney 2006, Australia;3. NHMRC Centre for Integrated Research and Understanding of Sleep (CIRUS), Woolcock Institute of Medical Research, Sydney 2037, Australia;4. Clinical Research Group, the Heart Research Institute, Sydney 2042, Australia;5. Department of Cardiology, Royal Prince Alfred Hospital, Sydney 2050, Australia;6. Division of Endocrinology, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA;7. Los Angeles Biomedical Research Institute, Harbor-UCLA Medical Center, Los Angeles, CA 90509, USA;1. Department of Thoracic Surgery, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu, China;2. Department of Public Health, Nantong University, Nantong 226001, Jiangsu, China;3. Department of Oncology, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu, China;4. Department of Gastroenterology, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu, China |
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| Abstract: | Nm23 was the first of what has become a field of over 20 known metastasis suppressor genes (MSGs). Since the discovery of Nm23 in 1988, a variety of mechanisms have been attributed to its activity, including a histidine kinase activity, binding of other proteins to regulate metastatic formation, and altered gene expression downstream of Nm23. Here, we will review current efforts to translate the previous work done on this MSG into the clinic, including high-dose medroxyprogesterone acetate (MPA), which has been shown to upregulate Nm23 expression. In addition, we will detail a new potential target downstream of Nm23. LPA1 is one of a group of known cell surface receptors for lysophosphatidic acid (LPA), which has been shown to be inversely correlated with Nm23 expression. A specific LPA1 antagonist could conceivably mimic the effects of Nm23 by downregulating the activity of the LPA1 pathway, which would be of considerable interest for potential clinical use. |
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