Jong-In Park, Ph.D.
Associate Professor
Dr. Park received his Bachelor’s and Master’s degrees in Biochemistry from Yonsei University, Seoul, Korea, and his Doctorate degree in Biochemistry and Molecular Genetics from the University of New South Wales, Sydney, Australia. The latter was awarded in 2000 for studies in Ras pathway-mediated stress responses. He was a postdoctoral fellow at the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University from 2000 to 2005 where he investigated tumor suppressive mechanisms activated by aberrant Ras/Raf/MEK/ERK signaling. Dr. Park joined the faculty of the Biochemistry Department at the Medical College of Wisconsin in 2006. Dr. Park’s research is currently supported by NIH-National Cancer Institute. Dr. Park is also a Research Scholar of American Cancer Society and a Young Clinical Scientist of Flight Attendant Medical Research Institute.
Contact Information
Phone: (414) 955-4098
Fax: (414) 955-6510
Email: jipark@mcw.edu
Research Interests
Proliferative programs of normal mammalian cells are interfaced with a variety of innate tumor-suppressive mechanisms that can trigger cell death or senescence in response to aberrant cell proliferation. Therefore, for carcinogenesis to occur, these defensive mechanisms must be inactivated.
The Ras and Raf families of oncogenes have been known for decades as transforming genes, and activation of the Raf/MEK/ERK pathway (the MAP kinase cascade of Ras) is a central signature of many epithelial cancers. However, paradoxically, aberrant activation of Ras or Raf elicits growth inhibitory effects, mainly characterized by cell cycle arrest and senescence, in primary cultured normal cells and in vivo. These responses are now appreciated as cellular innate defense mechanisms against Ras- and Raf-mediated tumorigenesis. Interestingly, the growth inhibitory effects of Ras/Raf/MEK/ERK activation are also observed in certain tumor cell lines in which the pathway signaling is not aberrant, suggesting that certain tumor cell types still possess the natural defense systems against aberrant activation of the pathway. Our overall goal is to understand by what mechanisms the Ras/Raf/MEK/ERK pathway mediates tumor suppressive signaling and to find a way to control the signaling, which may aid in designing novel therapeutic strategies.
Our research focuses include:
1. Investigating functional mechanisms of ERK required for mediating growth inhibition. We recently demonstrated, using molecular and cellular biological approaches, that ERK1/2 has a biochemical function other than its canonical kinase activity, which is utilized to mediate the Raf/MEK/ERK pathway-induced growth arrest. Current study focuses on identifying the mechanisms underlying this novel ERK signaling.
2. Identifying growth arrest specific regulators of MEK/ERK. We have developed a tandem affinity purification procedure to identify proteins interacting with MEK or ERK. Current study focuses on identifying MEK/ERK interacting proteins using this method and evaluating their involvement in the pathway-mediated growth inhibitory signaling.
3. Identifying cell-extrinsic growth inhibitory pathways of Ras/Raf/MEK/ERK. We previously identified, using column chromatography and proteomic mass spectrometry, leukemia inhibitory factor (LIF) as an autocrine/paracrine factor that can mediate cell-extrinsic growth inhibitory signaling of Ras/Raf/MEK/ERK in certain cancer types including medullary thyroid cancer and pheochromocytoma. Current focus is on evaluating therapeutic potential of LIF and identifying additional factors with therapeutic potential.
Recent Publications