Chengyu Liang, MD, PhD

Wistar Institute Professor of Biochemistry and Biophysics
Department: Biochemistry and Biophysics
Graduate Group Affiliations
Contact information
The Wistar Institute
3601 Spruce Street
Office 231 - Tower
Philadelphia, PA 19104
3601 Spruce Street
Office 231 - Tower
Philadelphia, PA 19104
Office: 215-898-3862
Lab: 215-898-3860
Lab: 215-898-3860
Email:
cliang@wistar.org
cliang@wistar.org
Education:
MD (Medicine)
Qingdao University School of Medicine, Qingdao, China, 1995.
MS (Genetics)
Peking Union Medical College& Chinese Academy of Medical Sciences , 1998.
MS (Computer Science)
State University of New York (SUNY) at Stony Brook, New York, 2004.
PhD (Molecular Genetics)
State University of New York (SUNY) at Stony Brook, New York, 2004.
Permanent linkMD (Medicine)
Qingdao University School of Medicine, Qingdao, China, 1995.
MS (Genetics)
Peking Union Medical College& Chinese Academy of Medical Sciences , 1998.
MS (Computer Science)
State University of New York (SUNY) at Stony Brook, New York, 2004.
PhD (Molecular Genetics)
State University of New York (SUNY) at Stony Brook, New York, 2004.
Description of Research Expertise
14. Expertise statementsThe homeostasis of all eukaryotic cells depends on their “greening” ability to use a lysosomal pathway known as autophagy to degrade and recycle self-components. Liang lab has identified and studied the mammalian essential autophagy protein, UV irradiation resistance associated gene (UVRAG), which functions in and beyond autophagy and has emerging significance in cancer research. Using a series of genetic, biochemical, molecular and cell biological, and computational approaches in model organisms from Drosophila to Zebrafish to mice, we have defined both canonical and non-degradative functions of UVRAG and the autophagy pathway in multiple endomembrane trafficking (Nat Cell Bio. 2006, 2008, 2013; PNAS 2018), in cell death control, in DNA damage repair, and in organelle homeostasis, and has linked a fundamental process to disease-causing pathological mechanisms. They have shown that UVRAG function and autophagy are inactivated by oncogenes such as cellular Bcl-2 and oncogenic γ-herpesvirus-encoded Bcl-2 proteins, by the oncogenic BRAF kinase, and by genetic mutations that increase inflammation and cancer susceptibility and can also be hitchhiked by viruses for their efficient infection.
Liang lab currently have several areas of focus:
•UVRAG in autophagy, inflammation, and cancer
•Autophagy-lysosomal activation in melanoma pathogenesis and drug resistance
•Molecular mechanisms of UV-indued mutagenesis in skin melanoma
•UV and tanning
•Chromosomal instability and cancer progression/recurrence
•Bcl-2 protein family in autophagy inhibition, cancer progression, and viral persistency
•Molecular mechanism of autophagy and intracellular membrane trafficking
Selected Publications
Choi, HY., Siddique. H., Zheng, M., Kou, Y., Yeh, DW., Machida, T., Chen, CL., Kumar, D., Punj, V., Winder, P., Pita, A., Sher, L., Tahara, S., Ray, RB., Liang, C., Chen, L., Tsukamoto, H., and Machida, K: destabilizing protein skews asymmetric division and enhances Notch activation to direct self-renewal of TICs. Nature Communications 11(1):3084, 2020.Li, S., Song, Y., Quach, C., Guo, H., Jang, G., Maazi, H., Zhao, S., Sands, N., Liu, Q., In, G., Peng, D., Yuan, W., Machida, K., Yu, M., Akbari, O., Hagiya, A., Yang, Y., Punj, V., Tang, L., and Liang, C*. : Transcriptional regulation of autophagy-lysosomal function in BRAF-driven melanoma progression and chemoresistance. Nature Communications 10(1):1693, 2019.
Guo, J., Jayaprakash, P., Dan, J., Wise, P., Jang, G., Liang, C., Chen, M., Woodley, D., Fabbri, M., and Li, W: PMC4519330. Molecular and Cellular Biology 37(19), 2017.
Minassian, A., Zhang, J, He, S., Zhao, J., Zandi, E., Saito, T., Liang, C., and Feng, P: An internally translated variant of MAVS exposes its amino-terminal TRAF-binding motifs to deregulate interferon induction. PLoS Pathogens 11(7): 110-120, 2015.
Pirooz, DS., He, S., Zhang, T., Zhao, Z., Oh, S., Amini-Bavil-Olyaee, S., Zhang, XW., Farzan, M., Huang, I-C., Liang, C*. : UVRAG is essential for endocytic virus entry through combinatorial interaction with the class C Vps complex and SNAREs. Proc Natl Acad Sci U S A 111 (7) , 2014.
He, S., Ni, D., Ma, B., Lee, JH., Zhang, T., Ghozalli, I., Pirooz, SD., Zhao, Z., Bharatham, N., Li, B., Oh, S., Lee, W-H., Takahashi, Y., Wang, H-G., Minassian, A., Feng, P., Deretic, V., Pepperkok, R., Tagaya, M., Yoon, HS., and Liang, C*: P-bound UVRAG coordinates Golgi-ER retrograde and Atg9 transport by differential interactions with the ER tether and the Beclin1 complex. Nature Cell Biology 15(10), 2013.
Zhao, Z., Oh, S., Ni, D., Pirooz, S., Li, D, Lee, JY, Lee, JH, Yang, S, Costanzo V, Stark, J, and Liang, C*: A dual role for UVRAG in maintaining chromosomal stability independent of autophagy. Developmental Cell 22(5): 1001-16, 2012.
Kliionsky DJ… Liang, C: Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes. Autophagy 8(9), 1392-1393 2012.
Pirooz, S., Lee, JH., Zhen, Z., Ni, D, Oh, S., and Liang, C: Measurement of γ-HV68 infection in mice. Cell Host and Microbe 11(2): 101-103, 2011.
Lee, G., Liang, C., Jang, C., Ohashi, H., Jung, JU and Chung, JK: Drosophila UVRAG mediates left-right axis rotation by regulating Notch endocytic degradation. Developmental Biology 356(2): 588-597, 2011.