Jong-In Park, PhD

Professor; Eminent Scholar

Locations

Biochemistry
BSB 357

Contact Information

General Interests

Oncogenic Cell Signaling, Metabolic Reprogramming in Cancer, Precision Medicine, Therapy Resistance

Education

Postdoc, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, 2005
PhD, University of New South Wales, Sydney, Australia, 2000
MA, Yonsei University, Seoul, Korea, 1990
BA, Yonsei University, Seoul, Korea, 1988

Biography

Dr. Park earned his Bachelor’s and Master’s degrees in Biochemistry and worked for the pharmaceutical branch of SAMSUNG, Inc until he decided to pursue an academic career. Dr. Park received his PhD degree in Biochemistry and Molecular Genetics for studies of Ras-regulated stress responses in yeast. He then conducted postdoctoral research on the role of the MAP kinase pathways for oncogenic Ras, Raf, and receptor tyrosine kinases in human cancer. Upon completing his training, Dr. Park joined the faculty of the Biochemistry Department at the Medical College of Wisconsin in 2006. Since then, Dr. Park has been studying oncogenic signaling and metabolic pathways in different tumors with the support from various funding agencies, including the NIH-National Cancer Institute, the American Cancer Society, and the Department of Defense.

In addition to basic science research, Dr. Park also conducts clinical cancer research. For example, since 2014, he has been participating in the NCI-MATCH Precision Medicine Cancer Trial as the Translational Chair of the Dabrafenib & Trametinib combination therapy arm, which targets BRAF-driven cancer. Dr. Park is a former recipient of the ACS Research Scholar award, the DOD New Investigator award, and the FAMRI Young Investigator award. At MCW, Dr. Park received multiple recognitions as Outstanding Medical Student Teacher and Outstanding Graduate Student Teacher.

Research Experience

Cell Cycle
Cell Death
Drug Resistance, Neoplasm
Gene Expression Regulation, Neoplastic
MAP Kinase Signaling System
Melanoma
Metabolism
Mitochondria
Molecular Chaperones
Pancreatic Neoplasms
Precision Medicine
Thyroid Neoplasms

Research Interests

Oncogenic transformation requires reprogramming in signaling and metabolism, which inevitably causes cellular stress that places pressure on transforming cells to develop stress tolerance mechanisms. As such, malignant tumors might have successfully developed a protective mechanism and, if identified, this mechanism may be targeted for therapy. An important goal of Park lab research is to elucidate the molecular mechanisms underlying these events and to translate the knowledge into an advanced therapeutic strategy.

Dr. Park’s research projects include:

Studying the role of mortalin in MEK/ERK-activated tumor cells

Jong-In Park Research Interests Image The MEK/ERK pathway is a key effector of the oncogenic BRAF, KRAS, and receptor tyrosine kinases, and its deregulation is a central signature of many epithelial cancers. We recently demonstrated that MEK/ERK deregulation puts cells at risk of mitochondrial cell death, but that mortalin, a mitochondrial chaperone, can counteract this risk. Briefly, mortalin can determine the live/die decision in MEK/ERK-dependent tumor cells by regulating a mitochondrial death machinery that consists of ANT, a mitochondrial channel that controls bioenergetic homeostasis, and CypD, a chaperone that functions as the gatekeeper of the mitochondrial permeability transition pore (view article PMID: 32156782; view article PMID: 32291414). Current studies in Park lab focus on elucidating the nature of mitochondrial stress associated with overactive MEK/ERK signaling in tumor cells and on identifying the molecular mechanisms by which mortalin protects tumor cells from this stress.

Targeting mitochondrial metabolism in RET-mutant cancers

Somatic as well as inherited mutations in the RET receptor tyrosine kinase are a key etiological factor in cancers, including thyroid cancer. For example, inherited RET mutations are an important prognostic marker for the multiple endocrine neoplasia type 2 (MEN2) syndrome, in which medullary thyroid cancer is a key pathological presentation. As a member of the American Cancer Society MEN2 consortium, we recently demonstrated that mitochondrial bioenergetics is affected by RET inhibition in medullary thyroid tumor cells and that the mitochondrial activity altered upon RET inhibition can be exploited for the design of a combination therapy with mitochondria targeted agents (view article PMID: 28475408). Our current research focuses on further developing this concept in different tumors.

Participating 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 (view article PMID: 32758030). Find more information at the National Cancer Institute.

ERK1/2 interaction with DHPS regulates eIF5A deoxyhypusination independently of ERK kinase activity.

(Becker AE, Kochanowski P, Wu PK, Wątor E, Chen W, Guchhait K, Biela AP, Grudnik P, Park JI.) Cell Rep. 2024 Oct 22;43(10):114831 PMID: 39392755 PMCID: PMC11544350 SCOPUS ID: 2-s2.0-85207351264 10/11/2024
Estrogen-related receptor alpha promotes thyroid tumor cell survival via a tumor subtype-specific regulation of target gene networks.

(Chen W, Song YS, Lee HS, Lin CW, Lee J, Kang YE, Kim SK, Kim SY, Park YJ, Park JI.) Oncogene. 2024 Jul;43(31):2431-2446 PMID: 38937602 PMCID: PMC11629884 SCOPUS ID: 2-s2.0-85197858420 06/28/2024
Erlotinib combination with a mitochondria-targeted ubiquinone effectively suppresses pancreatic cancer cell survival.

(Leung PY, Chen W, Sari AN, Sitaram P, Wu PK, Tsai S, Park JI.) World J Gastroenterol. 2024 Feb 21;30(7):714-727 PMID: 38515951 PMCID: PMC10950623 SCOPUS ID: 2-s2.0-85185579019 03/22/2024
Selpercatinib combination with the mitochondria-targeted antioxidant MitoQ effectively suppresses RET-mutant thyroid cancer.

(Chen W, Dream S, Leung PY, Wu PK, Wong S, Park JI.) NPJ Precis Oncol. 2024 Feb 20;8(1):39 PMID: 38378752 PMCID: PMC10879150 SCOPUS ID: 2-s2.0-85185513016 02/21/2024
Tumor Cell Resistance to the Inhibition of BRAF and MEK1/2.

(Chen W, Park JI.) Int J Mol Sci. 2023 Oct 02;24(19) PMID: 37834284 PMCID: PMC10573597 SCOPUS ID: 2-s2.0-85174308251 10/14/2023
Effects of Subnormothermic Regulated Hepatic Reperfusion on Mitochondrial and Transcriptomic Profiles in a Porcine Model.

(Kim J, Zimmerman MA, Shin WY, Boettcher BT, Lee JS, Park JI, Ali M, Yang M, Mishra J, Hagen CE, McGraw JE, Mathison A, Woehlck HJ, Lomberk G, Camara AKS, Urrutia RA, Stowe DF, Hong JC.) Ann Surg. 2023 Feb 01;277(2):e366-e375 PMID: 34387201 PMCID: PMC8840998 SCOPUS ID: 2-s2.0-85146161896 08/14/2021
Prolonged warm ischemia time increases mitogen-activated protein kinase activity and decreases perfusate cytokine levels in ex vivo rat liver machine perfusion.

(Kim J, Hong SK, Yang Y, Lee A, Hoffmeister KM, Gantner BN, Park JI.) Front Transplant. 2023;2:1215182 PMID: 38993858 PMCID: PMC11235240 SCOPUS ID: 2-s2.0-85204385238 07/12/2024
MAPK-ERK Pathway

(Park JI.) International Journal of Molecular Sciences. June 2023;24(11) SCOPUS ID: 2-s2.0-85161598318 06/01/2023
Editorial: The role of mortalin in biology and disease

(Park JI.) Frontiers in Cell and Developmental Biology. 2023;11 SCOPUS ID: 2-s2.0-85153495202 01/01/2023
Analogs of the Heat Shock Protein 70 Inhibitor MKT-077 Suppress Medullary Thyroid Carcinoma Cells.

(Hong SK, Starenki D, Johnson OT, Gestwicki JE, Park JI.) Int J Mol Sci. 2022 Jan 19;23(3) PMID: 35162987 PMCID: PMC8835675 SCOPUS ID: 2-s2.0-85122962789 02/16/2022
eIF5A-Independent Role of DHPS in p21CIP1 and Cell Fate Regulation.

(Becker AE, Wu PK, Park JI.) Int J Mol Sci. 2021 Dec 07;22(24) PMID: 34947982 PMCID: PMC8707118 SCOPUS ID: 2-s2.0-85120635476 12/25/2021
Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

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