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Chengyu Liang, M.D., Ph.D., serves as the Christopher M. David Professor and Program Co-Leader of the Molecular and Cellular Oncogenesis Program in the Ellen and Ronald Caplan Cancer Center at The Wistar Institute. She also holds the title of Wistar Institute Professor of Biochemistry and Biophysics. Liang joined Wistar in 2020 after serving as a tenured associate professor in the Department of Molecular Microbiology and Immunology at the University of Southern California Keck School of Medicine, where she founded her independent laboratory in 2009. Earlier, she conducted postdoctoral research in tumor virology at Harvard Medical School's Department of Microbiology and Molecular Genetics. Her academic training includes an M.D. from Qingdao University School of Medicine in 1995, an M.S. in Genetics from Peking Union Medical College and Chinese Academy of Medical Sciences in 1998, an M.S. in Computer Science in 2004, and a Ph.D. in Molecular Genetics in 2004 from the State University of New York at Stony Brook.
Liang's research elucidates fundamental cellular mechanisms underlying inflammation, infection, and cancer, with particular emphasis on autophagy, organelle homeostasis, genomic stability, membrane trafficking, and virus-host interactions. Her laboratory pioneered the identification of UVRAG as a multifunctional autophagic tumor suppressor with roles in coordinating autophagic, endocytic, secretory, and melanogenic pathways, thereby linking membrane dynamics to cellular stress responses, metabolic control, and disease processes. The lab integrates genetic, biochemical, molecular, and cell biological approaches in models including Drosophila, zebrafish, and mice to explore UVRAG functions in endomembrane trafficking, cell death control, DNA damage repair, and organelle homeostasis. Key publications include "Kaposi’s sarcoma-associated herpesvirus induces mitochondrial fission to evade host immune responses and promote viral production" (Nature Microbiology, 2025), "Transcriptional regulation of autophagy-lysosomal function in BRAF-driven melanoma progression and chemoresistance" (Nature Communications, 2019), "Autophagic and tumour suppressor activity of a novel Beclin1-binding protein UVRAG" (Nature Cell Biology, 2006), "TRIM25 RING-finger E3 ubiquitin ligase is essential for RIG-I-mediated antiviral activity" (Nature, 2007), and "Beclin1-binding UVRAG targets the class C Vps complex to coordinate autophagosome maturation and endocytic trafficking" (Nature Cell Biology, 2008). These works have shaped understanding of autophagy's intersection with oncogenesis, therapy resistance, and antiviral immunity.