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Jungwhan (Jay) Kim, D.V.M., PhD
Oncology Science

Jungwhan Kim, D.V.M., PhD

Associate Professor

1122 NE 13th St, ORB 335B, Oklahoma City, OK 73117

405.271.8001 Ext. 35023


Post Doc., University of California, San Diego (USCD) / Salk Institute, La Jolla, CA

Ph.D., Johns Hopkins University, School of Medicine, Baltimore, MD

D.V.M., Konkuk University, College of Veterinary Medicine, Seoul, Korea

Clinical/Research Interests:

  • Mechanisms underlying glucose reliance and metabolic vulnerabilities in squamous cell carcinomas
  • Fibroblast metabolic reprogramming and plasticity in pancreatic cancer and fibrotic diseases
  • Dietary Intervention for cancer therapeutics
  • Integrated comparative oncology to develop novel therapeutic modalities for human and veterinary cancer patients

Research Projects

Glucose reliance and metabolic vulnerabilities in human SCC
Despite intensive efforts, targeting augmented glucose metabolism has resulted in varied, unsatisfactory outcomes to be considered as a viable therapeutic option for further development. Among multiple factors preventing effective therapeutic responses, a poorly understood tumor-intrinsic metabolic heterogeneity across different cancers, arising potentially from diverse microenvironmental or lineage-specific factors, may preclude effective therapeutic strategies to target cancer metabolism. In our recently published study, we uncovered the molecular mechanism in which, a squamous lineage-specific program p63 and SOX2 promotes GLUT1 expression through the intronic enhancer transactivation of the SLC2A1 (that encodes GLUT1) in human squamous cell carcinomas. This previously unrecognized metabolic feature embedded in squamous cancers argue that remarkably heightened GLUT1 expression and glucose influx is not a uniform metabolic hallmark of all cancers, but a potent and unique characteristic of squamous lineage cancers. We are studying epigenetic and molecular events underlying this control mechanism by characterizing how various transcription factors are binding and transcriptional activities within and across the locus and its boundaries enable SLC2A1 overexpression in SCC. The overarching goal of this project is to develop novel ways to silence the SLC2A1 gene selectively in SCC.

Metabolic reprogramming and plasticity in the tumor microenvironment and fibrotic diseases
Metabolic dysregulation in stromal cells is associated with various human diseases including cancer and fibrosis. We previously reported that fibroblastic hypoxic signaling plays critical roles in tumor growth, tumor vascular remodeling, and therapeutic responses. In addition, our group has demonstrated that genetic as well as pharmacological inhibition of hypoxia-inducible factor-1 (HIF-1)-mediated metabolic reprogramming significantly attenuate the progression of interstitial pulmonary fibrosis. Our studies suggest a critical biological and clinical consideration for evaluating metabolic alterations in myofibroblast activation and fibrotic progression in the tumor microenvironment and fibrotic progression. We employ various transgenic animal model systems for an integrated understanding of cellular and molecular mechanistic link between metabolic alterations and plasticity and accelerated myofibroblastic activation and differentiation in highly desmoplastic cancers (e.g. pancreatic cancer) as well as pulmonary fibrosis.

Dietary intervention for cancer therapeutics
A growing body of evidence has demonstrated that dietary modulation could improve the response to cancer therapy. Given that cancers display diverse metabolic requirements influenced by numerous factors such as intrinsic oncogenic alterations, microenvironmental components, and therapeutic intervention, individualized strategies are essential for effective targeting metabolic vulnerabilities of specific cancer via dietary intervention. We have shown that ketogenic diet specifically inhibited the development of lung squamous cancers in KrasG12D;LKB1-null (KL) of human non-small cell lung cancer (NSCLC) model as well as esophagus, head and neck squamous cancer xenograft tumor models. We further demonstrated that the anti-SCC effects of ketogenic diet is due to systemic glucose restriction and an associated suppression of insulin/PI3K/AKT signaling in SCC cells. We are exploring combinatorial regimens to improve therapeutic efficacy of ketogenic diet and other dietary modulations. In addition, we are studying the impact of systemic responses by dietary intervention on stromal components such as immune cells in the tumor microenvironment.

Select Publications:

Hsieh MH, Choe JH, Gadhvi J, Kim YJ, Arguez MA, Palmer M, Gerold H, Nowak C, Do H, Mazambani S, Knighton JK, Cha M, Goodwin J, Kang MK, Jeong JY, Lee SY, Faubert B, Xuan Z, Abel ED, Scafoglio C, Shackelford DB, Minna JD, Singh PK, Shulaev V, Bleris L, Hoyt K, Kim J, Inoue M, DeBerardinis RJ, Kim TH, Kim JW*. p63 and SOX2 Dictate Glucose Reliance and Metabolic Vulnerabilities in Squamous Cell Carcinomas. Cell Reports. 2019;28(7):1860-78 e9. doi: 10.1016/j.celrep.2019.07.027. PubMed PMID: 31412252; PMCID: PMC7048935.

Abe H, Takeda N, Isagawa T, Semba H, Nishimura S, Morioka MS, Nakagama Y, Sato T, Soma K, Koyama K, Wake M, Katoh M, Asagiri M, Neugent ML, Kim JW, Stockmann C, Yonezawa T, Inuzuka R, Hirota Y, Maemura K, Yamashita T, Otsu K, Manabe I, Nagai R, Komuro I. Macrophage hypoxia signaling regulates cardiac fibrosis via Oncostatin M. Nature Communications. 2019;10(1):2824. doi: 10.1038/s41467-019-10859-w. PubMed PMID: 31249305; PMCID: PMC6597788.

Goodwin J, Choi H, Hsieh MH, Neugent ML, Ahn JM, Hayenga HN, Singh PK, Shackelford DB, Lee IK, Shulaev V, Dhar S, Takeda N, Kim JW*. Targeting Hypoxia-Inducible Factor-1alpha/Pyruvate Dehydrogenase Kinase 1 Axis by Dichloroacetate Suppresses Bleomycin-induced Pulmonary Fibrosis. Am J Respir Cell Mol Biol. 2018;58(2):216-31. doi: 10.1165/rcmb.2016-0186OC. PubMed PMID: 28915065; PMCID: PMC5805994.

Shukla SK, Purohit V, Mehla K, Gunda V, Chaika NV, Vernucci E, King RJ, Abrego J, Goode GD, Dasgupta A, Illies AL, Gebregiworgis T, Dai B, Augustine JJ, Murthy D, Attri KS, Mashadova O, Grandgenett PM, Powers R, Ly QP, Lazenby AJ, Grem JL, Yu F, Mates JM, Asara JM, Kim JW, Hankins JH, Weekes C, Hollingsworth MA, Sarkova NJ, Sasson AR, Fleming JB, Oliveto JM, Lyssiotis CA, Cantley LC, Berim L, Singh PK. MUC1 and HIF-1alpha Signaling Crosstalk Induces Anabolic Glucose Metabolism to Impart Gemcitabine Resistance to Pancreatic Cancer. Cancer Cell. 2017;32(1):71-87 e7. doi: 10.1016/j.ccell.2017.06.004. PubMed PMID: 28697344; PMCID: PMC5533091.

Goodwin J, Neugent ML, Lee SY, Choe JH, Choi H, Jenkins DMR, Ruthenborg RJ, Robinson MW, Jeong JY, Wake M, Abe H, Takeda N, Endo H, Inoue M, Xuan Z, Yoo H, Chen M, Ahn JM, Minna JD, Helke KL, Singh PK, Shackelford DB, Kim JW*. The distinct metabolic phenotype of lung squamous cell carcinoma defines selective vulnerability to glycolytic inhibition. Nature Communications. 2017;8:15503. doi: 10.1038/ncomms15503. PubMed PMID: 28548087.

Semba H, Takeda N, Isagawa T, Sugiura Y, Honda K, Wake M, Miyazawa H, Yamaguchi Y, Miura M, Jenkins DM, Choi H, Kim JW, Asagiri M, Cowburn AS, Abe H, Soma K, Koyama K, Katoh M, Sayama K, Goda N, Johnson RS, Manabe I, Nagai R, Komuro I. HIF-1alpha-PDK1 axis-induced active glycolysis plays an essential role in macrophage migratory capacity. Nature Communications. 2016;7:11635. doi: 10.1038/ncomms11635. PubMed PMID: 27189088; PMCID: PMC4873978.

Oh ET^, Kim JW^, Kim JM, Kim SJ, Lee JS, Hong SS, Goodwin J, Ruthenborg RJ, Jung MG, Lee HJ, Lee CH, Park ES, Kim C, Park HJ. NQO1 inhibits proteasome-mediated degradation of HIF-1alpha. Nature Communications. 2016;7:13593. doi: 10.1038/ncomms13593. PubMed PMID: 27966538; PMCID: PMC5171868. (^ Co-First Authors)

Lee YS^, Kim JW^, Osborne O, Oh da Y, Sasik R, Schenk S, Chen A, Chung H, Murphy A, Watkins SM, Quehenberger O, Johnson RS, Olefsky JM. Increased adipocyte O2 consumption triggers HIF-1alpha, causing inflammation and insulin resistance in obesity. Cell. 2014;157(6):1339-52. doi: 10.1016/j.cell.2014.05.012. PubMed PMID: 24906151; PMCID: 4114226. (^ Co-First Authors)

Kim JW, Evans C, Weidemann A, Takeda N, Lee YS, Stockmann C, Branco-Price C, Brandberg F, Leone G, Ostrowski MC, Johnson RS. Loss of fibroblast HIF-1alpha accelerates tumorigenesis. Cancer Research. 2012;72(13):3187-95. doi: 10.1158/0008-5472.CAN-12-0534. PubMed PMID: 22556263; PMCID: 4089958.

Kim JW, Tchernyshyov I, Semenza GL, Dang CV. HIF-1-mediated expression of pyruvate dehydrogenase kinase: a metabolic switch required for cellular adaptation to hypoxia. Cell Metabolism. 2006;3(3):177-85. doi: 10.1016/j.cmet.2006.02.002. PubMed PMID: 16517405.

Complete List of Publications:
MyNCBI, Google Scholar