Dongsun Lee

Dr. Dongsun Lee

Faculty of Biotechnology, College of Applied Life Sciences, Jeju National University, Jeju, Korea
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Research Focus & Metrics

Academic Career Length

25Years (2002-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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Journal Article
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LKLing-Zu Kong
Ling-Zu Kong
NCNisansala Chandimali
Nisansala Chandimali
YHYing-Hao Han
Ying-Hao Han
DLDong-Ho Lee
Dong-Ho Lee
JKJi-Su Kim
Ji-Su Kim
Taeho KwonTaeho Kwon
Taeho Kwon
Alcoholic liver disease (ALD) refers to the damages to the liver and its functions due to alcohol overconsumption. It consists of fatty liver/steatosis, alcoholic hepatitis, steatohepatitis, chronic hepatitis with liver fibrosis or cirrhosis, and hepatocellular carcinoma. However, the mechanisms behind the pathogenesis of alcoholic liver disease are extremely complicated due to the involvement of immune cells, adipose tissues, and genetic diversity. Clinically, the diagnosis of ALD is not yet well developed. Therefore, the number of patients in advanced stages has increased due to the failure of proper early detection and treatment. At present, abstinence and nutritional therapy remain the conventional therapeutic interventions for ALD. Moreover, the therapies which target the TNF receptor superfamily, hormones, antioxidant signals, and MicroRNAs are used as treatments for ALD. In particular, mesenchymal stem cells (MSCs) are gaining attention as a potential therapeutic target of ALD. Therefore, in this review, we have summarized the current understandings of the pathogenesis and diagnosis of ALD. Moreover, we also discuss the various existing treatment strategies while focusing on promising therapeutic approaches for ALD.

18 July 2018 in Molecular Carcinogenesis
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HCHack Sun Choi
Hack Sun Choi
JKJi‐Hyang Kim
Ji‐Hyang Kim
SKSu‐Lim Kim
Su‐Lim Kim
HDHong‐Yuan Deng
Hong‐Yuan Deng
DLDoseung Lee
Doseung Lee
DLDongsun Lee
Dongsun Lee

24 March 2019 in Oxidative Medicine and Cellular Longevity
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SKSu-Lim Kim
Su-Lim Kim
HCHack Sun Choi
Hack Sun Choi
JKJi-Hyang Kim
Ji-Hyang Kim
DJDong Kee Jeong
Dong Kee Jeong
KKKi-Seok Kim
Ki-Seok Kim
DLDongsun Lee
Dongsun Lee
Cancer stem cells (CSCs) are known to mediate metastasis and recurrence and are therefore a promising therapeutic target. In this study, we found that dihydrotanshinone (DHTS) inhibits CSC formation. DHTS inhibited mammosphere formation in a dose-dependent manner and showed significant tumor growth inhibition in a xenograft model. This compound reduced the CD44high/CD24low- and aldehyde dehydrogenase- (ALDH-) expressing cell population and the self-renewal-related genes Nanog, SOX2, OCT4, C-Myc, and CD44. DHTS induced NOX5 activation by increasing calcium, and NOX5 activation induced reactive oxygen species (ROS) production. ROS production reduced the nuclear phosphorylation levels of Stat3 and secreted IL-6 levels in the mammospheres. DHTS deregulated the dynamic equilibrium from non-stem cancer cells to CSCs by dephosphorylating Stat3 and decreasing IL-6 secretion and inhibiting CSC formation. These novel findings showed that DHTS-induced ROS deregulated the Stat3/IL-6 pathway and induced CSC death. NOX5 activation by DHTS inhibits CSC formation through ROS/Stat3/IL-6 signaling, and DHTS may be a promising potential therapeutic agent against breast CSCs.

10 October 2019 in Cancers
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JKJi-Hyang Kim
Ji-Hyang Kim
HCHack sun Choi
Hack sun Choi
SKSu-Lim Kim
Su-Lim Kim
DLDongsun Lee
Dongsun Lee
Cancer stem cells (CSCs) have unique properties, including self-renewal, differentiation, and chemoresistance. In this study, we found that p21-activated kinase (PAK1) inhibitor (Group I, PAK inhibitor, IPA-3) and inactivator (ivermectin) treatments inhibit cell proliferation and that tumor growth of PAK1-knockout cells in a mouse model is significantly reduced. IPA-3 and ivermectin inhibit CSC formation. PAK1 physically interacts with Janus Kinase 2 (JAK2), and JAK2 inhibitor (TG101209) treatment inhibits mammosphere formation and reduces the nuclear PAK1 protein level. PAK1 interacts with signal transducer and activator of transcription 3 (Stat3), and PAK1 and Stat3 colocalize in the nucleus. We show through electrophoretic mobility shift assay (EMSA), chromatin immunoprecipitation (ChIP), and reporter assays that the PAK1/Stat3 complex binds to the IL-6 promoter and regulates the transcription of the IL-6 gene. Inhibition of PAK1 and JAK2 in mammospheres reduces the nuclear pStat3 and extracellular IL-6 levels. PAK1 inactivation inhibits CSC formation by decreasing pStat3 and extracellular IL-6 levels. Our results reveal that JAK2/PAK1 dysregulation inhibits the Stat3 signaling pathway and CSC formation, the PAK1/Stat3 complex regulates IL-6 gene expression, PAK1/Stat3 signaling regulates CSC formation, and PAK1 may be an important target for treating breast cancer.

3 June 2020 in Molecules
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YKYu-Chan Ko
Yu-Chan Ko
HCHack sun Choi
Hack sun Choi
RLRen Liu
Ren Liu
JKJi-Hyang Kim
Ji-Hyang Kim
SKSu-Lim Kim
Su-Lim Kim
DLDongsun Lee
Dongsun Lee
Breast cancer stem cells (BCSCs) are responsible for tumor chemoresistance and recurrence. Targeting CSCs using natural compounds is a novel approach for cancer therapy. A CSC-inhibiting compound was purified from citrus extracts using silica gel, gel filtration and high-pressure liquid chromatography. The purified compound was identified as tangeretin by using nuclear magnetic resonance (NMR). Tangeretin inhibited cell proliferation, CSC formation and tumor growth, and modestly induced apoptosis in CSCs. The frequency of a subpopulation with a CSC phenotype (CD44+/CD24−) was reduced by tangeretin. Tangeretin reduced the total level and phosphorylated nuclear level of signal transducer and activator of transcription 3 (Stat3). Our results in this study show that tangeretin inhibits the Stat3 signaling pathway and induces CSC death, indicating that tangeretin may be a potential natural compound that targets breast cancer cells and CSCs.

15 March 2024 in Ageing Research Reviews
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Journal Article
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MAMeraj Ansari
Meraj Ansari
MGMrinmoy Ghosh
Mrinmoy Ghosh
DLDongsun Lee
Dongsun Lee
Youngok SonYoungok Son
Youngok Son