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author Yang, Liquan
Chen, Guangchun
Mohanty, Sonali
Scott, Glynis
Fazal, Fabeha
Rahman, Arshad
Begum, Shahinoor
Hynes, Richard O
Xu, Lei,S.M.Massachusetts Institute of Technology.
author2 Massachusetts Institute of Technology. Department of Biology
author_facet Massachusetts Institute of Technology. Department of Biology
Yang, Liquan
Chen, Guangchun
Mohanty, Sonali
Scott, Glynis
Fazal, Fabeha
Rahman, Arshad
Begum, Shahinoor
Hynes, Richard O
Xu, Lei,S.M.Massachusetts Institute of Technology.
author_sort Yang, Liquan
collection MIT
description 2012 February 15
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institution Massachusetts Institute of Technology
language en_US
last_indexed 2024-09-23T11:31:41Z
publishDate 2012
publisher American Association for Cancer Research
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spelling mit-1721.1/736722022-09-27T20:06:22Z GPR56 Regulates VEGF Production and Angiogenesis during Melanoma Progression Yang, Liquan Chen, Guangchun Mohanty, Sonali Scott, Glynis Fazal, Fabeha Rahman, Arshad Begum, Shahinoor Hynes, Richard O Xu, Lei,S.M.Massachusetts Institute of Technology. Massachusetts Institute of Technology. Department of Biology Koch Institute for Integrative Cancer Research at MIT Begum, Shahinoor Hynes, Richard O. 2012 February 15 Angiogenesis is a critical step during cancer progression. The VEGF is a major stimulator for angiogenesis and is predominantly contributed by cancer cells in tumors. Inhibition of the VEGF signaling pathway has shown promising therapeutic benefits for cancer patients, but adaptive tumor responses are often observed, indicating the need for further understanding of VEGF regulation. We report that a novel G protein–coupled receptor, GPR56, inhibits VEGF production from the melanoma cell lines and impedes melanoma angiogenesis and growth, through the serine threonine proline-rich segment in its N-terminus and a signaling pathway involving protein kinase Cα. We also present evidence that the two fragments of GPR56, which are generated by autocatalyzed cleavage, played distinct roles in regulating VEGF production and melanoma progression. Finally, consistent with its suppressive roles in melanoma progression, the expression levels of GPR56 are inversely correlated with the malignancy of melanomas in human subjects. We propose that components of the GPR56-mediated signaling pathway may serve as new targets for antiangiogenic treatment of melanoma. Cancer Res; 71(16); 5558–68. National Institutes of Health (U.S.) (U54CA126515) Howard Hughes Medical Institute 2012-10-09T14:34:30Z 2012-10-09T14:34:30Z 2011-07 2011-06 Article http://purl.org/eprint/type/JournalArticle 0008-5472 1538-7445 http://hdl.handle.net/1721.1/73672 Yang, L. et al. “GPR56 Regulates VEGF Production and Angiogenesis During Melanoma Progression.” Cancer Research 71.16 (2011): 5558–5568. https://orcid.org/0000-0001-7603-8396 en_US http://dx.doi.org/10.1158/0008-5472.CAN-10-4543 Cancer Research Creative Commons Attribution-Noncommercial-Share Alike 3.0 http://creativecommons.org/licenses/by-nc-sa/3.0/ application/pdf American Association for Cancer Research PMC
spellingShingle Yang, Liquan
Chen, Guangchun
Mohanty, Sonali
Scott, Glynis
Fazal, Fabeha
Rahman, Arshad
Begum, Shahinoor
Hynes, Richard O
Xu, Lei,S.M.Massachusetts Institute of Technology.
GPR56 Regulates VEGF Production and Angiogenesis during Melanoma Progression
title GPR56 Regulates VEGF Production and Angiogenesis during Melanoma Progression
title_full GPR56 Regulates VEGF Production and Angiogenesis during Melanoma Progression
title_fullStr GPR56 Regulates VEGF Production and Angiogenesis during Melanoma Progression
title_full_unstemmed GPR56 Regulates VEGF Production and Angiogenesis during Melanoma Progression
title_short GPR56 Regulates VEGF Production and Angiogenesis during Melanoma Progression
title_sort gpr56 regulates vegf production and angiogenesis during melanoma progression
url http://hdl.handle.net/1721.1/73672
https://orcid.org/0000-0001-7603-8396
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