The Shuyang Chen lab studies the biology of melanoma and other skin diseases. We investigate how genetic factors, cellular metabolism, and interactions with the immune system influence disease development and progression, with the goal of improving prevention and treatment strategies.
Dr. Shuyang Chen is an Assistant Staff in the Department of Cancer Biology at Cleveland Clinic and an Assistant Professor at Cleveland Clinic Lerner College of Medicine (CCLCM) of Case Western Reserve University (CWRU).
Ph.D. in Biological Science, Drexel University, Philadelphia, PA
B.S. in Biological Science, University of Science and Technology of China, Hefei, China
Our laboratory studies the fundamental mechanisms that drive melanoma and other skin diseases. We aim to understand how genetic susceptibility, cellular signaling, metabolism, and immune responses interact to control disease initiation, progression, and therapeutic response.
A central goal of our research is to uncover how diverse signaling pathways regulate key biological processes such as pigmentation, genomic stability, cellular metabolism, and communication between tumor cells and the immune system. These processes are essential for maintaining normal skin homeostasis but can be disrupted during disease development to promote tumor growth and immune evasion.
Our previous work has revealed important links between pigmentation signaling, metabolic regulation, and melanoma susceptibility, with discoveries published in journals including Nature, Nature Communications, Cancer Research, and the Journal of Clinical Investigation. Building on these findings, our lab continues to explore how molecular signaling networks shape tumor–immune interactions and disease progression.
To address these questions, we combine genetic and molecular approaches with emerging human-relevant models, including human skin organoids, advanced mouse models, and patient-derived systems. We also integrate single-cell and spatial multi-omics, functional genomics, and molecular profiling to dissect disease mechanisms across multiple biological scales.
By bridging fundamental discovery with human disease models, our goal is to identify new strategies for preventing melanoma and improving therapies for patients with melanoma and other skin diseases.
Selected publications:
1. Li H, Lyu J, Sun Y, Yin C, Li Y, Chen W, Foo SS, Wu X, Goding CR, Chen S. S-acyl transferase ZDHHC13 modulates tumor microenvironment interactions to suppress metastasis in melanoma models. J Clin Invest. 2025 Dec 1;135(23). doi: 10.1172/JCI188249. eCollection 2025 Dec 1. PubMed PMID: 41321310; PubMed Central PMCID: PMC12646662.
2. Sun Y, Li X, Yin C, Zhang J, Liang E, Wu X, Ni Y, Arbesman J, Goding CR, Chen S. AMPK phosphorylates ZDHHC13 to increase MC1R activity and suppress melanomagenesis. Cancer Res. 2023 Jan 26; PubMed PMID: 36701140.
3. Park J, Zhao Y, Zhang F, Zhang S, Kwong AC, Zhang Y, Hoffmann HH, Bushweller L, Wu X, Ashbrook AW, Stefanovic B, Chen S, Branch AD, Mason CE, Jung JU, Rice CM, Wu X. IL-6/STAT3 axis dictates the PNPLA3-mediated susceptibility to non-alcoholic fatty liver disease. J Hepatol. 2023 Jan;78(1):45-56. doi: 10.1016/j.jhep.2022.08.022. PubMed PMID: 36049612; PubMed Central PMCID: PMC9772150.
4. Yin C, Zhu B, Zhang T, Liu T, Chen S, Liu Y, Li X, Miao X, Li S, Mi X, Zhang J, Li L, Wei G, Xu ZX, Gao X, Huang C, Wei Z, Goding CR, Wang P, Deng X, Cui R. Pharmacological Targeting of STK19 Inhibits Oncogenic NRAS-Driven Melanomagenesis. Cell. 2019 Feb 21;176(5):1113-1127.e16. doi: 10.1016/j.cell.2019.01.002. Epub 2019 Jan 31. PubMed PMID: 30712867.
5. Chen S, Han C, Miao X, Li X, Yin C, Zou J, Liu M, Li S, Stawski L, Zhu B, Shi Q, Xu ZX, Li C, Goding CR, Zhou J, Cui R. Targeting MC1R depalmitoylation to prevent melanomagenesis in redheads. Nat Commun. 2019 Feb 20;10(1):877. doi: 10.1038/s41467-019-08691-3. PubMed PMID: 30787281; PubMed Central PMCID: PMC6382811.
6. Zhu B, Tang L, Chen S, Yin C, Peng S, Li X, Liu T, Liu W, Han C, Stawski L, Xu ZX, Zhou G, Chen X, Gao X, Goding CR, Xu N, Cui R, Cao P. Targeting the upstream transcriptional activator of PD-L1 as an alternative strategy in melanoma therapy. Oncogene. 2018 Sep;37(36):4941-4954. doi: 10.1038/s41388-018-0314-0. Epub 2018 May 22. PubMed PMID: 29786078.
7. Zhu B, Chen S, Wang H, Yin C, Han C, Peng C, Liu Z, Wan L, Zhang X, Zhang J, Lian CG, Ma P, Xu ZX, Prince S, Wang T, Gao X, Shi Y, Liu D, Liu M, Wei W, Wei Z, Pan J, Wang Y, Xuan Z, Hess J, Hayward NK, Goding CR, Chen X, Zhou J, Cui R. The protective role of DOT1L in UV-induced melanomagenesis. Nat Commun. 2018 Jan 17;9(1):259. doi: 10.1038/s41467-017-02687-7. PubMed PMID: 29343685; PubMed Central PMCID: PMC5772495.
8. Chen S, Zhu B, Yin C, Liu W, Han C, Chen B, Liu T, Li X, Chen X, Li C, Hu L, Zhou J, Xu ZX, Gao X, Wu X, Goding CR, Cui R. Palmitoylation-dependent activation of MC1R prevents melanomagenesis. Nature. 2017 Sep 21;549(7672):399-403. doi: 10.1038/nature23887. Epub 2017 Sep 6. PubMed PMID: 28869973; PubMed Central PMCID: PMC5902815.
9. Robles-Espinoza CD, Roberts ND, Chen S, Leacy FP, Alexandrov LB, Pornputtapong N, Halaban R, Krauthammer M, Cui R, Timothy Bishop D, Adams DJ. Germline MC1R status influences somatic mutation burden in melanoma. Nat Commun. 2016 Jul 12;7:12064. doi: 10.1038/ncomms12064. PubMed PMID: 27403562; PubMed Central PMCID: PMC4945874.
Our education and training programs offer hands-on experience at one of the nationʼs top hospitals. Travel, publish in high impact journals and collaborate with investigators to solve real-world biomedical research questions.
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