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Gil, Minchan,Pak, Hyo-Kyung,Park, Seo-Jeong,Lee, A-Neum,Park, Young-Soo,Lee, Hyangsin,Lee, Hyunji,Kim, Kyung-Eun,Lee, Kyung Jin,Yoon, Dok Hyun,Chung, Yoo-Sam,Park, Chan-Sik 한국조명·전기설비학회 2015 한국조명·전기설비학회 학술대회논문집 Vol. No.
<P>CD99 signaling is crucial to a diverse range of biological functions including survival and proliferation. CD99 engagement is reported to augment activator protein-1 (AP-1) activity through mitogen-activated protein (MAP) kinase pathways in a T-lymphoblastic lymphoma cell line Jurkat and in breast cancer cell lines. In this study, we report that CD99 differentially regulated AP-1 activity in the human myeloma cell line RPMI8226. CD99 was highly expressed and the CD99 engagement led to activation of the MAP kinases, but suppressed AP-1 activity by inducing the expression of basic leucine zipper transcription factor, ATF-like (BATF), a negative regulator of AP-1 in RPMI8226 cells. By contrast, engagement of CD99 enhanced AP-1 activity and did not change the BATF expression in Jurkat cells. CD99 engagement reduced the proliferation of RPMI8226 cells and expression of cyclin 1 and 3. Overall, these results suggest novel CD99 functions in RPMI8226 cells.</P>
Interleukin‐15 enhances proliferation and chemokine secretion of human follicular dendritic cells
Gil, Minchan,Park, Seo‐,Jeong,Chung, Yoo‐,Sam,Park, Chan‐,Sik Blackwell Publishing Ltd 2010 Immunology Vol.130 No.4
<P><B>Summary</B></P><P>The germinal centre (GC) is a specialized microenvironment where high‐affinity antibodies are produced through hypermutation and isotype switching. Follicular dendritic cells (FDCs) are the stromal cells of the GC. The timely expansion and establishment of an FDC network is essential for a protective GC reaction; however, only a few factors modulating FDC development have been recognized. In this study, we report that interleukin‐15 (IL‐15) enhances human primary FDC proliferation and regulates cytokine secretion. The FDCs express IL‐15 receptor complexes for IL‐15 signal transduction as well as for specific binding. Moreover, the secretion of chemokines CCL‐2, CCL‐5, CXCL‐5 and CXCL‐8 was reduced by blocking IL‐15 signalling while the secretion of other cytokines, and the expression of CD14, CD44, CD54 (ICAM‐1) and CD106 (VCAM‐1) proteins remained unchanged. These results suggest that IL‐15 plays a crucial role in the development of FDC networks during GC reaction, offering a new target for immune modulation.</P>
Gil, Minchan,Kim, Yun Kyu,kim, Ha Yeong,Pak, Hyo-Kyung,Park, Chan-Sik,Lee, Kyung Jin Elsevier 2018 Biochemical and biophysical research communication Vol.495 No.1
<P><B>Abstract</B></P> <P>Cereblon (CRBN) has a pleiotropic role in important cellular processes and is a potential therapeutic target in several diseases, including mental retardation, cancer, and metabolic disorders. The role of CRBN in polymicrobial sepsis induced by cecal ligation and puncture (CLP) was investigated using CRBN-deficient (KO) mice. Survival following CLP was significantly higher in KO mice compared to wild-type (WT) controls (50% vs 0% at day 6 after CLP). The improved survival of KO mice was accompanied by reduced peripheral blood bacterial load and lung injury. Serum tumor necrosis factor (TNF)-α and high mobility group box 1 (HMGB1) concentrations were significantly lower in KO mice than in WT mice. Peritoneal macrophages from KO mice with CLP-induced septic mouse had higher levels of activation of AMPK and heme oxygenase-1 (HO-1). Forced expression of CRBN in macrophage of KO mice suppressed activation of 5′ adenosine monophosphate-activated protein kinase (AMPK) and HO-1 and augmented expression of TNF-α and HMGB1 as inhibition of AMPK by compound C. These studies demonstrate the contribution of CRBN expression to the pathogenesis of CLP-induced sepsis and peritoneal macrophage responses and suggest a novel therapeutic modality for polymicrobial sepsis.</P>
Gil, Minchan,Kim, Yun Kye,Kim, Kyung-Eun,Kim, Wook,Park, Chan-Sik,Lee, Kyung Jin Elsevier 2016 Biochemical and biophysical research communication Vol.470 No.1
<P><B>Abstract</B></P> <P>Function of cellular prion protein (PrP<SUP>c</SUP>) in cancer progression has not been elucidated yet. Ectopic expression of PrP<SUP>c</SUP> increases the invasion and migration of breast cancer cell line, MCF-7 cells. Overexpressed PrP<SUP>c</SUP> increases matrix metalloprotease-9 (MMP-9) expression by enhancing association of NF-κB in promoter of MMP-9 gene and ERK signaling in MCF-7 cells. Whereas, silencing of PrP<SUP>c</SUP> by siRNA suppresses ERK activation and MMP-9 expression resulting the down-regulation of MD-MB231 cell migration and invasion. Overall, these results suggest that PrP<SUP>c</SUP> contribute the breast cancer invasion and migration via MMP-9.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Cellular prion protein (PrP<SUP>c</SUP>) increases invasion of breast cancer cells. </LI> <LI> PrP<SUP>c</SUP> induces MMP-9 activity through activation of NF-kB pathway. </LI> <LI> Activation of ERK is involved in increase of MMP-9 by PrP<SUP>c</SUP>. </LI> </UL> </P>
Prognostic role of EGR1 in breast cancer: a systematic review
( Subbroto Kumar Saha ),( S. M. Riazul Islam ),( Tripti Saha ),( Afsana Nishat ),( Polash Kumar Biswas ),( Minchan Gil ),( Lewis Nkenyereye ),( Shaker El-sappagh ),( Saiful Islam ),( Ssang-goo Cho ) 생화학분자생물학회 2021 BMB Reports Vol.54 No.10
EGR1 (early growth response 1) is dysregulated in many cancers and exhibits both tumor suppressor and promoter activities, making it an appealing target for cancer therapy. Here, we used a systematic multi-omics analysis to review the expression of EGR1 and its role in regulating clinical outcomes in breast cancer (BC). EGR1 expression, its promoter methylation, and protein expression pattern were assessed using various publicly available tools. COSMIC-based somatic mutations and cBioPortal-based copy number alterations were analyzed, and the prognostic roles of EGR1 in BC were determined using Prognoscan and Kaplan-Meier Plotter. We also used bc-GenEx-Miner to investigate the EGR1 co-expression profile. EGR1 was more often downregulated in BC tissues than in normal breast tissue, and its knockdown was positively correlated with poor survival. Low EGR1 expression levels were also associated with increased risk of ER+, PR+, and HER2- BCs. High positive correlations were observed among EGR1, DUSP1, FOS, FOSB, CYR61, and JUN mRNA expression in BC tissue. This systematic review suggested that EGR1 expression may serve as a prognostic marker for BC patients and that clinicopathological parameters influence its prognostic utility. In addition to EGR1, DUSP1, FOS, FOSB, CYR61, and JUN can jointly be considered prognostic indicators for BC. [BMB Reports 2021; 54(10): 497-504]
Tussilagone Inhibits the Inflammatory Response and Improves Survival in CLP-Induced Septic Mice
Kim, Yun Kyu,Yeo, Myeong Gu,Oh, Bo Kang,Kim, Ha Yeong,Yang, Hun Ji,Cho, Seung-Sik,Gil, Minchan,Lee, Kyung Jin MDPI 2017 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.18 No.12
<P>Tussilagone, extracted from <I>Tussilago farfara</I> is an oriental medicine used for asthma and bronchitis. We investigated its mechanism of action, its inhibitory effects on lipopolysaccharide-induced inflammation in macrophages, and its impact on viability in a cecal ligation and puncture (CLP)-induced mouse model of sepsis. Tussilagone suppressed the expression of the inflammatory mediators, nitric oxide and prostaglandin E2, and the inflammatory cytokines, tumor necrosis factor-alpha (TNF-α) and high-mobility group box 1 (HMGB1), in lipopolysaccharide-stimulated RAW 264.7 cells and peritoneal macrophages. Tussilagone also reduced the activation of the mitogen-activated protein kinases and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) involved in the activation of various inflammatory mediators in activated macrophages. Moreover, tussilagone administration (1 mg/kg and 10 mg/kg) produced decreased mortality and lung injury in CLP-activated septic mice. Augmented expression of cyclooxygenase (COX)-2 and TNF-α in pulmonary alveolar macrophages of septic mice were attenuated by tussilagone administration. Tussilagone also suppressed the induction of nitric oxide, prostaglandin E2, TNF-α and HMGB1 in the serum of the septic mice. Overall, tussilagone exhibited protective effects against inflammation and polymicrobial sepsis by suppressing inflammatory mediators possibly via the inhibition of NF-κB activation and the MAP kinase pathway. These results suggest the possible use of tussilagone for developing novel therapeutic modalities for sepsis and other inflammatory diseases.</P>