Seunghwan Lim, PhD

Senior Research Associate
Department of Pediatrics
School of Medicine

Research Information

Research Interests

Dr. Lim earned a PhD degree at SUNY Upstate Medical University. As part of his thesis work, he discovered a novel gene named as DCoHm (AF499009), which is a transcription cofactor of hepatocyte nuclear factor 1 (HNF1). He continued to pursue the study of cell survival mechanisms as a postdoctoral researcher in the Laboratory of Cell Regulation and Carcinogenesis at the NCI/NIH, delineating how inflammatory cytokine-mediated cell survival is regulated by TGF-β signaling in normal and cancer cells. Dr. Lim found a novel mechanism that apoptosis or cell growth arrest induced by the TGF-β signaling is diminished by TNF-receptor activated factor 6 (TRAF6).

Since his transition to Case Western Reserve University, Dr. Lim has developed several lines of research related to targeting tumor metastasis and overcoming therapy resistance. First, he has developed a high-throughput drug screening system for identification of niche-directed therapeutic targets using a unique three-dimensional osteoblastic niche (3D-ObN). The capacity of the 3D-ObN to mimic the in vivo osteoblastic niche has been validated by its ability to recapitulate the homing mechanisms of hematopoietic stem cells (HSCs). Now, the 3D-ObN assay is used for understanding previously unknown mechanisms occurring during cellular interactions between bone metastatic tumors and the bone marrow niche. Second, he has made significant contributions to studies that have revealed a novel function of Cdk5 in melanomagenesis and progression, utilizing a new B-RafV600E/Pten/Cdk5 genetically engineered mouse model. There are currently significant research efforts toward the development of novel CDK5-specific inhibitors for clinical applications. Lastly, he is involved in developing cell-mediated therapeutic strategies targeting 1) immune cells and tumor interaction in the tumor microenvironment and 2) the propensity of cancer cells to home to sites of metastasis, which is known as the ‘self-seeding’ mechanism. He hopes these research efforts will lead to expanded therapeutic modalities for cancer patients whose options are otherwise limited.

Publications