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Name:	Jing Chen
Position:	Associate Professor of Hematology and Medical Oncology
Degree:	Ph.D., Emory University, 2001
Programs:	MSP, Full Member CB, Full Member
Phone:	404 778-5274
Address:	3002 Winship Cancer Inst, 1701 Uppergate Dr, 1751/001/1CD
Email:	jchen@emory.edu
Research Descriptions:
Short:	Role of post-translational modifications including phosphorylation, acetylation and ubiquitination in human cancers, with a particular focus on oncogenesis, metastasis and cancer metabolism.
Long:	We are interested in exploration of the signaling network of leukemogenic tyrosine kinase that regulate leukemogenesis and disease progression, and translate the insights obtained in basic research to clinical applications. One of the major focus in this direction to address the long standing question - does the Ph+ leukemia phenotype depend on the features of BCR-ABL, the target cell type, or both? One hypothesis is that the signaling properties of the target cancer-initiating stem cells provide the ¿right¿ signaling network for BCR-ABL-induced transformation to give rise to either myeloid or lymphoid leukemia. These studies will provide alternative target for curative therapy of human Ph+ leukemias. The Warburg effect describes an interesting metabolism switch that cancer cells take up more glucose than normal tissue, yet use less glucose for energy production and favor a much less efficient metabolic mechanism called glycolysis. It remains unknown how crucial this is for initiation and disease progression in human cancers. We approached these questions by examining whether tyrosine kinase signaling ¿ commonly upregulated in tumors ¿ regulates the Warburg effect to contribute to tumorigenesis and maintenance of the tumor. Our ultimate hypothesis is that oncogenic tyrosine kinases phosphorylates a spectrum of metabolic enzymes to promote the Warburg effect and tumorigenesis by reprogramming cancer cell metabolism in an acute way, in addition to the long-term changes that are believed to be regulated by hypoxia inducible factor 1 (HIF-1) and Myc. Metastasis is the most dangerous switch during tumor progression from a locally growing tumor to a deadly killer, which is the cause of 90% of deaths from cancer. We are currently using combined approaches of cell culture-based studies, murine models of diseases, genome-wide screening and proteomics analyses developed in our leukemia research as platforms to identify and characterize pro-metastatic oncogenes and signaling effectors in solid tumors. Recent publications: Kang, S., Dong, S., Gu, T., Guo,A., Cohen, M.S., Lonial, S., Khoury, H.J., Fabbro, D., Gilliland, D. G., Bergsagel, P.L., Taunton, J., Polakiewicz, R.D., and Chen, J. (2007) FGFR3 activates RSK2 to mediate hematopoietic transformation through both tyrosine phosphorylation of RSK2 and activation of the MEK/ERK pathway. Cancer Cell 12(3):201-14 Hitosugi, T., Kang, S., Chung, T.-W., Vander Heiden, M.G., Elf, S., Lythgoe, K., Dong, S., Lonial, S., Wang, X., Chen, G.Z., Xie, J., Gu, T.-L., Polakiewicz, R.D., Roesel, J.L., Boggon, T.J., Gilliland, D.G., Cantley, L.C., Kaufman, J., and Chen, J. (2009) Tyrosine phosphorylation inhibits PKM2 to promote the Warburg effect and tumor growth. Science Signaling 2009 Nov 17, 2(97) ra73 Kang, S., Elf, S., Lythgoe, K., Hitosugi, T., Taunton, J., Zhou, W., Xiong, L., Wang, D., Muller, S., Fan, S., Sun, S.-Y., Marcus, A.I., Gu, T.-L., Polakiewicz, R.D., Chen, G.Z., Khuri, F.R., Shin, D.M., and Chen, J. (2010) RSK2 promotes head and neck cancer cell invasion and tumor metastasis. J Clin Invest 120(4):1165-77.