Staff Collaborate Conference Room

Jong-In Park, PhD

Jong-In Park

Jong-In Park, PhD



  • Biochemistry
    BSB 357

Contact Information


BA and MBioch, Yonsei University, Seoul, Korea
PhD, University of New South Wales, Sydney, Australia, 2000


Dr. Park earned a PhD in Biochemistry and Molecular Genetics from the University of New South Wales, Sydney, Australia in 2000 for studies in Ras pathway-mediated stress responses.& His postdoctoral training in Cancer Biology was completed at the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University in 2005. Previously, he earned Bachelor’s and Master’s degrees in Biochemistry from Yonsei University, Seoul, Korea, and worked for the pharmaceutical branch of SAMSUNG, Inc. He joined the faculty of the Biochemistry Department at the Medical College of Wisconsin in 2006.

Dr. Park’s current basic cancer research programs are supported by the NIH-National Cancer Institute and the American Cancer Society (ACS). He also participates in clinical cancer research by serving the NCI-MATCH Precision Medicine Cancer Trial as the Translational Chair of the Dabrafenib & Trametinib combination therapy arm, which targets BRAF-driven cancer. He is currently an ACS Research Scholar and a member of the ACS MEN2 Thyroid Cancer Consortium.

Research Interests

Proliferative programs of normal mammalian cells are interfaced with a variety of, so called, “innate tumor-suppressive mechanisms” that can trigger growth arrest or cell death in response to aberrant cell proliferation signals such as oncogenic mutations. Therefore, for carcinogenesis to occur, these mechanisms must be inactivated (A model is depicted at right). This inactivation usually requires reprogramming of signaling and metabolic pathways. parksignalingmodelVery intriguingly, certain oncogene-associated tumor suppressive mechanisms can be reactivated in cancer, providing a rationale for the design of a strategy to trigger “synthetic lethality” in cancer. The primary goal of our research is to understand the molecular mechanisms underlying these events and to translate the knowledge into an advanced therapeutic strategy.

Our current research focuses include:

Investigating the role of mortalin/GRP75/HSPA9 in Ras/Raf-transformed cancer. The Ras and Raf families of oncogenes have been known for decades as transforming genes, and activation of the Raf/MEK/ERK pathway 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 a variety of cell types and in vivo. These responses are appreciated as innate tumor defense mechanisms against Ras- and Raf-mediated tumorigenesis. We recently demonstrated that mortalin, a mitochondrial molecular chaperone often upregulated in cancers, can determine cell fate in the face of oncogenic Ras/Raf mutations. Importantly, mortalin depletion or inhibition reactivated the tumor suppressive mechanisms associated with Raf/MEK/ERK in cancer cells. Current studies, supported by the NIH/NCI, focus on further elucidating the molecular and biochemical mechanisms underlying mortalin-regulated signaling and metabolic pathways. Moreover, we evaluate therapeutic potential of small molecule inhibitors relevant in this context.

Investigating oncogenic signaling pathways and mitochondrial metabolism in thyroid cancer. Somatic as well as inherited mutations in the RET receptor tyrosine kinase are a key etiological factor for thyroid cancer. Further, inherited RET mutations are an important prognostic marker for the multiple endocrine neoplasia type 2 (MEN2) syndrome, wherein medullary thyroid cancer is a key pathological presentation. As a member of the American Cancer Society MEN2 consortium, we study the underlying molecular and biochemical mechanisms altered in thyroid cancer. We recently demonstrated that metabolic reprogramming in mitochondria is critical for medullary thyroid cancer cell survival and RET expression, thus proposing mitochondria as a potential therapeutic target for this tumor. Our current research further evaluates therapeutic potential of targeting mitochondrial metabolism in thyroid cancer.

Participation in the NCI-MATCH Precision Medicine Cancer Trial. This clinical trial is a “genotype to phenotype” phase II study. An important goal of this study is to identify the features of various tumor types with the same mutation that cause them to either respond to or resist treatment with a targeted therapy. More information is available at the NCI-Molecular Analysis for Therapy Choice (NCI-MATCH) Trial Website.


  • Dabrafenib and Trametinib in Patients With Tumors With BRAFV600E Mutations: Results of the NCI-MATCH Trial Subprotocol H.

    (Salama AKS, Li S, Macrae ER, Park JI, Mitchell EP, Zwiebel JA, Chen HX, Gray RJ, McShane LM, Rubinstein LV, Patton D, Williams PM, Hamilton SR, Armstrong DK, Conley BA, Arteaga CL, Harris LN, O'Dwyer PJ, Chen AP, Flaherty KT.) J Clin Oncol. 2020 Aug 06:JCO2000762 PMID: 32758030 08/08/2020

  • Anticholestatic Effect of Bardoxolone Methyl on Hepatic Ischemia-reperfusion Injury in Rats.

    (Kim J, Hagen CE, Kumar SN, Park JI, Zimmerman MA, Hong JC.) Transplant Direct. 2020 Aug;6(8):e584 PMID: 32766432 PMCID: PMC7371100 08/09/2020

  • Growth Inhibitory Signaling of the Raf/MEK/ERK Pathway.

    (Wu PK, Becker A, Park JI.) Int J Mol Sci. 2020 Jul 30;21(15) PMID: 32751750 PMCID: PMC7432891 SCOPUS ID: 2-s2.0-85089131301 08/06/2020

  • Mortalin/HSPA9 targeting selectively induces KRAS tumor cell death by perturbing mitochondrial membrane permeability.

    (Wu PK, Hong SK, Starenki D, Oshima K, Shao H, Gestwicki JE, Tsai S, Park JI.) Oncogene. 2020 May;39(21):4257-4270 PMID: 32291414 PMCID: PMC7244387 SCOPUS ID: 2-s2.0-85083767959 04/16/2020

  • Mortalin (HSPA9) facilitates BRAF-mutant tumor cell survival by suppressing ANT3-mediated mitochondrial membrane permeability.

    (Wu PK, Hong SK, Chen W, Becker AE, Gundry RL, Lin CW, Shao H, Gestwicki JE, Park JI.) Sci Signal. 2020 Mar 10;13(622) PMID: 32156782 PMCID: PMC7099430 SCOPUS ID: 2-s2.0-85081677231 03/12/2020

  • Mortalin (GRP75/HSPA9) Promotes Survival and Proliferation of Thyroid Carcinoma Cells.

    (Starenki D, Sosonkina N, Hong SK, Lloyd RV, Park JI.) Int J Mol Sci. 2019 Apr 26;20(9) PMID: 31027376 PMCID: PMC6540051 SCOPUS ID: 2-s2.0-85065295769 04/28/2019

  • Treatment of Cells and Tissues with Chromate Maximizes Mitochondrial 2Fe2S EPR Signals.

    (Antholine WE, Vasquez-Vivar J, Quirk BJ, Whelan HT, Wu PK, Park JI, Myers CR.) Int J Mol Sci. 2019 Mar 06;20(5) PMID: 30845710 PMCID: PMC6429069 SCOPUS ID: 2-s2.0-85062628835 03/09/2019

  • A cellular threshold for active ERK1/2 levels determines Raf/MEK/ERK-mediated growth arrest versus death responses.

    (Hong SK, Wu PK, Park JI.) Cell Signal. 2018 Jan;42:11-20 PMID: 28986121 PMCID: PMC5732048 SCOPUS ID: 2-s2.0-85031106212 10/08/2017

  • Steady-State Levels of Phosphorylated Mitogen-Activated Protein Kinase Kinase 1/2 Determined by Mortalin/HSPA9 and Protein Phosphatase 1 Alpha in KRAS and BRAF Tumor Cells.

    (Wu PK, Hong SK, Park JI.) Mol Cell Biol. 2017 Sep 15;37(18) PMID: 28674184 PMCID: PMC5574043 SCOPUS ID: 2-s2.0-85028363255 07/05/2017

  • Vandetanib and cabozantinib potentiate mitochondria-targeted agents to suppress medullary thyroid carcinoma cells.

    (Starenki D, Hong SK, Wu PK, Park JI.) Cancer Biol Ther. 2017 Jul 03;18(7):473-483 PMID: 28475408 PMCID: PMC5639831 SCOPUS ID: 2-s2.0-85020693671 05/06/2017

  • Suppression of B-RafV600E melanoma cell survival by targeting mitochondria using triphenyl-phosphonium-conjugated nitroxide or ubiquinone.

    (Hong SK, Starenki D, Wu PK, Park JI.) Cancer Biol Ther. 2017 02;18(2):106-114 PMID: 27786591 PMCID: PMC5362989 SCOPUS ID: 2-s2.0-85013783900 10/28/2016

  • Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).

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