Research Scientist, Kennedy Krieger Institute
Phone: 443-923-9498
Kennedy Krieger Institute

707 N. Broadway
Baltimore, MD 21205
United States


Shuli Xia is a research scientist at the Kennedy Krieger Institute. She is also an Associate Professor in the Departments of Neurology at the Johns Hopkins University School of Medicine.


Dr. Xia received her doctoral degree in biology from Johannes-Gutenberg University in Mainz, Germany. She had her post-doctoral training at Washington University School of Medicine in St. Louis, MO and Yale University School of Medicine in New Haven, CT before she came to the Kennedy Krieger Institute in 2002. She became a faculty member at the Kennedy Krieger Institute in 2006.


Dr. Xia's research focuses on understanding the genetic and epigenetic mechanisms of brain tumor malignancy, including tumor proliferation/survival, invasion and the tumor microenvironment. The ultimate goal of her research is to develop novel anti-tumor therapeutic strategies to treat brain malignancy.

(A). Functional analysis of DNA methylation in brain tumor malignancy

A study to discover in the impact of DNA methylation on brain tumor cell gene expression and phenotype changes. We established a new paradigm, by which DNA methylation, a well-accepted repressive epigenetic mark, directs transcription factor binding in a sequence-specific manner. The study found that the transcription factor kruppel-like factor 4 (KLF4) interacts with methylated DNA in promoter and enhancer regions to activate gene expression, thereby influencing cellular behaviors including migration, differentiation and mitochondrial function. Heterozygous mutations in isocitrate dehydrogenase 1 (IDH1) are among the earliest and most common genetic alterations during gliomagenesis. IDH1 mutations generate a neomorphic enzyme activity that converts α-ketoglutarate to D-2-hydroxyglutarate, leading to the inhibition of more than 80 dioxygenases, and consequently global epigenetic alterations including DNA hypermethylation. By employing a highly efficient “single base editing” technique, we established multiple isogeneic cellular models carrying heterozygous IDH1R132/WT. Global genetic and epigenetic analyses reveal that mutant IDH1 modulates interaction between tumor cells and immune cells.

(B). Mechanism of glioma cell migration/invasion

Brain tumor cell migration and infiltration contribute to tumor recurrence. Researchers established an innovative dual-fluorescence approach to study brain tumor migration and invasion in vivo by co-injecting control and experimental cells labeled with different fluorescent dyes. This novel method establishes a rigorous and efficient approach to study tumor invasion regulation in vivo, and at the same time reduced the number of animals needed for invasion studies. Using this method, we investigated the role of EphB2 receptor in glioblastoma proliferation/migration dichotomy. Researchers also determined function of extracellular matrix proteins in brain tumor migration.

(C). Signaling transduction pathways and glioma cell death

Researchers are interested in employing various combinatory strategies to selectively induce glioma cell death, including radiation, chemotherapeutic drugs, tyrosine kinase inhibitors, death receptor ligands, histone deacetylase inhibitors and synolytic drugs. In addition, researchers are interested in targeting glioma stem cells.

Related Links

Elsevier Fingerprint Engine Profile for Shuli Xia

Google Scholar Profile

Research Publications

Uzoma I, Hu J, Cox E, Xia S, Zhou J, Rho HS, Guzzo C, Paul C, Ajala O, Goodwin CR, Jeong J, Moore C, Zhang H, Meluh P, Blackshaw S, Matunis M, Qian J, Zhu H (2018). Global Identification of SUMO Substrates Reveals Crosstalk between SUMOylation and Phosphorylation Promotes Cell Migration. Mol Cell Proteomics. ,.