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Search Results: 1 - 10 of 26015 matches for " Dae-Ghon Kim1 "
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Genome-wide expression patterns associated with oncogenesis and sarcomatous transdifferentation of cholangiocarcinoma
Min-A Seol, In-Sun Chu, Mi-Jin Lee, Goung-Ran Yu, Xiang-Dan Cui, Baik-Hwan Cho, Eun-Kyung Ahn, Sun-Hee Leem, In-Hee Kim, Dae-Ghon Kim
BMC Cancer , 2011, DOI: 10.1186/1471-2407-11-78
Abstract: Genes that were differentially expressed between CC cell lines or tissues and cultured normal biliary epithelial (NBE) cells were identified using DNA microarray technology. Expressions were validated in human CC tissues and cells.Using unsupervised hierarchical clustering analysis of the cell line and tissue samples, we identified a set of 342 commonly regulated (>2-fold change) genes. Of these, 53, including tumor-related genes, were upregulated, and 289, including tumor suppressor genes, were downregulated (<0.5 fold change). Expression of SPP1, EFNB2, E2F2, IRX3, PTTG1, PPARγ, KRT17, UCHL1, IGFBP7 and SPARC proteins was immunohistochemically verified in human and hamster CC tissues. Additional unsupervised hierarchical clustering analysis of sarcomatoid CC cells compared to three adenocarcinomatous CC cell lines revealed 292 differentially upregulated genes (>4-fold change), and 267 differentially downregulated genes (<0.25 fold change). The expression of 12 proteins was validated in the CC cell lines by immunoblot analysis and immunohistochemical staining. Of the proteins analyzed, we found upregulation of the expression of the epithelial-mesenchymal transition (EMT)-related proteins VIM and TWIST1, and restoration of the methylation-silenced proteins LDHB, BNIP3, UCHL1, and NPTX2 during sarcomatoid transdifferentiation of CC.The deregulation of oncogenes, tumor suppressor genes, and methylation-related genes may be useful in identifying molecular targets for CC diagnosis and prognosis.Cholangiocarcinoma (CC) is a highly lethal adenocarcinoma arising from bile duct epithelial cells. CC accounts for approximately 15% of the total liver cancer cases worldwide, and its incidence is rising [1,2]. The prognosis for CC is quite poor because of difficulties in early diagnosis, and relative resistance of the tumors to chemotherapy [3,4]. At the time of diagnosis, approximately 70% of CC patients have an occult metastasis or advanced local disease that precludes curativ
Anti-fibrotic effects of L-2-oxothiazolidine-4-carboxylic acid via modulation of nuclear factor erythroid 2-related factor 2 in rats
In Hee Kim1,2, Dae-Ghon Kim1,2*, Peipei Hao2, Yunpeng Wang2, Seong Hun Kim1,2, Sang Wook Kim1,2, Seung Ok Lee1,2 & Soo Teik Lee1,2
BMB Reports , 2012,
Abstract: L-2-Oxothiazolidine-4-carboxylic acid (OTC) is a cysteine prodrugthat maintains glutathione in tissues. The present studywas designed to investigate anti-fibrotic and anti-oxidative effectsof OTC via modulation of nuclear factor erythroid 2-relatedfactor 2 (Nrf2) in an in vivo thioacetamide (TAA)-inducedhepatic fibrosis model. Treatment with OTC (80 or 160 mg/kg)improved serum liver function parameters and significantlyameliorated liver fibrosis. The OTC treatment groups exhibitedsignificantly lower expression of α-smooth muscle actin, transforminggrowth factor-β1, and collagen α1 mRNA than that inthe TAA model group. Furthermore, the OTC treatment groupsshowed a significant decrease in hepatic malondialdehyde levelcompared to that in the TAA model group. Nrf2 and hemeoxygenase-1 expression increased significantly in the OTCtreatment groups compared with that in the TAA model group.Taken together, these results suggest that OTC restores the anti-oxidative system by upregulating Nrf2; thus, ameliorating liverinjury and a fibrotic reaction.
Frequent Amplification of CENPF, GMNN and CDK13 Genes in Hepatocellular Carcinomas
Hye-Eun Kim, Dae-Ghon Kim, Kyung Jin Lee, Jang Geun Son, Min-Young Song, Young-Mi Park, Jae-Jung Kim, Sung-Won Cho, Sung-Gil Chi, Hyun Sub Cheong, Hyoung Doo Shin, Sang-Wook Lee, Jong-Keuk Lee
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0043223
Abstract: Genomic changes frequently occur in cancer cells during tumorigenesis from normal cells. Using the Illumina Human NS-12 single-nucleotide polymorphism (SNP) chip to screen for gene copy number changes in primary hepatocellular carcinomas (HCCs), we initially detected amplification of 35 genes from four genomic regions (1q21–41, 6p21.2–24.1, 7p13 and 8q13–23). By integrated screening of these genes for both DNA copy number and gene expression in HCC and colorectal cancer, we selected CENPF (centromere protein F/mitosin), GMNN (geminin, DNA replication inhibitor), CDK13 (cyclin-dependent kinase 13), and FAM82B (family with sequence similarity 82, member B) as common cancer genes. Each gene exhibited an amplification frequency of ~30% (range, 20–50%) in primary HCC (n = 57) and colorectal cancer (n = 12), as well as in a panel of human cancer cell lines (n = 70). Clonogenic and invasion assays of NIH3T3 cells transfected with each of the four amplified genes showed that CENPF, GMNN, and CDK13 were highly oncogenic whereas FAM82B was not. Interestingly, the oncogenic activity of these genes (excluding FAM82B) was highly correlated with gene-copy numbers in tumor samples (correlation coefficient, r>0.423), indicating that amplifications of CENPF, GMNN, and CDK13 genes are tightly linked and coincident in tumors. Furthermore, we confirmed that CDK13 gene copy number was significantly associated with clinical onset age in patients with HCC (P = 0.0037). Taken together, our results suggest that coincidently amplified CDK13, GMNN, and CENPF genes can play a role as common cancer-driver genes in human cancers.
PEP-1-p18 prevents neuronal cell death by inhibiting oxidative stress and Bax expression
Duk-Soo Kim2,#, Eun Jeong Sohn1,#, Dae Won Kim1, Young Nam Kim1, Seon Ae Eom1, Ga Hyeon Yoon1, Sung-Woo Cho3, Sang-Hyun Lee1, Hyun Sook Hwang1, Yoon Shin Cho1, Jinseu Park1, Won Sik Eum1,* & Soo Young Choi1,*
BMB Reports , 2012,
Abstract: P18, a member of the INK4 family of cyclin-dependent kinaseinhibitors, is a tumor suppressor protein and plays a key cellsurvival role in a variety of human cancers. Under pathophysiologicalconditions, the INK4 group proteins participate in novelbiological functions associated with neuronal diseases andoxidative stress. Parkinson’s disease (PD) is characterized by loss ofdopaminergic neurons, and oxidative stress is important in itspathogenesis. Therefore, we examined the effects of PEP-1-p18 onoxidative stress-induced SH-SY5Y cells and in a PD mouse model.The transduced PEP-1-p18 markedly inhibited 1-methyl-4-phenylpyridinium-induced SH-SY5Y cell death by inhibiting Baxexpression levels and DNA fragmentation. Additionally, PEP-1-p18prevented dopaminergic neuronal cell death in the substantia nigraof a 1-methyl-4-phenyl-1,2,3,6,-tetrahydropyridine-induced PDmouse model. These results indicate that PEP-1-p18 may be auseful therapeutic agent against various diseases and is a potentialtool for treating PD.
Suppression of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin inflammation in mice by transduced Tat-Annexin protein
Sun Hwa Lee1,#, Dae Won Kim1,#, Seon Ae Eom1, Se-Young Jun1, Meeyoung Park1, Duk-Soo Kim2, Hyung Joo Kwon3, Hyeok Yil Kwon4, Kyu Hyung Han1, Jinseu Park1, Hyun Sook Hwang1, Won Sik Eum1,* & Soo Young Choi1,*
BMB Reports , 2012,
Abstract: We examined that the protective effects of ANX1 on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin inflammationin animal models using a Tat-ANX1 protein. Topicalapplication of the Tat-ANX1 protein markedly inhibited TPAinducedear edema and expression levels of cyclooxygenase-2(COX-2) as well as pro-inflammatory cytokines such as interleukin-1 beta (IL-1β), IL-6, and tumor necrosis factor-alpha(TNF-α). Also, application of Tat-ANX1 protein significantlyinhibited nuclear translocation of nuclear factor-kappa B(NF-κB) and phosphorylation of p38 and extracellular signalregulatedkinase (ERK) mitogen-activated protein kinase(MAPK) in TPA-treated mice ears. The results indicate thatTat-ANX1 protein inhibits the inflammatory response byblocking NF-κB and MAPK activation in TPA-induced miceears. Therefore, the Tat-ANX1 protein may be useful as atherapeutic agent against inflammatory skin diseases.
Human milk oligosaccharides: the novel modulator of intestinal microbiota
Kyunghun Jeong1, Vi Nguyen2 & Jaehan Kim1,*
BMB Reports , 2012,
Abstract: Human milk, which nourishes the early infants, is a source ofbioactive components for the infant growth, development andcommensal formulation as well. Human milk oligosaccharide is agroup of complex and diverse glycans that is apparently notabsorbed in human gastrointestinal tract. Although mostmammalian milk contains oligosaccharides, oligosaccharides inhuman milk exhibit unique features in terms of their types,amounts, sizes, and functionalities. In addition to the preventionof infectious bacteria and the development of early immunesystem, human milk oligosaccharides are able to facilitate thehealthy intestinal microbiota. Bifidobacterial intestinal microbiotaappears to be established by the unilateral interaction betweenmilk oligosaccharides, human intestinal activity and commensals.Digestibility, membrane transportation and catabolic activity bybacteria and intestinal epithelial cells, all of which are linked tothe structural of human milk oligosaccharides, are crucial indetermining intestinal microbiota.
IFNγ-mediated inhibition of cell proliferation through increased PKCδ-induced overexpression of EC-SOD
Yoon-Jae Jeon1, Hyun Yoo1, Byung Hak Kim1, Yun Sang Lee1, Byeongwook Jeon1, Sung-Sub Kim2,* & Tae-Yoon Kim1,*
BMB Reports , 2012,
Abstract: Extracellular superoxide dismutase (EC-SOD) overexpressionmodulates cellular responses such as tumor cell suppression andis induced by IFNγ. Therefore, we examined the role of EC-SODin IFNγ-mediated tumor cell suppression. We observed that thedominant-negative protein kinase C delta (PKCδ) suppressesIFNγ-induced EC-SOD expression in both keratinocytes andmelanoma cells. Our results also showed that PKCδ-induced ECSODexpression was reduced by pretreatment with a PKCspecificinhibitor or a siRNA against PKCδ. PKCδ-induced ECSODexpression suppressed cell proliferations by the up-regulationof p21 and Rb, and the downregulation of cyclin A and D.Finally, we demonstrated that increased expression of EC-SODdrastically suppressed lung melanoma proliferation in an EC-SODtransgenic mouse via p21 expression. In summary, our findingssuggest that IFNγ-induced EC-SOD expression occurs via activationof PKCδ. Therefore, the upregulation of EC-SOD may beeffective for prevention of various cancers, including melanoma,via cell cycle arrest.
AMP-activated protein kinase: implications on ischemic diseases
Yong-Joo Ahn1,#, Hwewon Kim1,#, Heejin Lim2, Max Lee1, Yuhyun Kang1, SangJun Moon2, Hyeon Soo Kim3 & Hyung-Hwan Kim1,*
BMB Reports , 2012,
Abstract: Ischemia is a blockage of blood supply due to an embolism ora hemorrhage in a blood vessel. When an organ cannot receiveoxygenated blood and can therefore no longer replenish itsblood supply due to ischemia, stresses, such as the disruptionof blood glucose homeostasis, hypoglycemia and hypoxia,activate the AMPK complex. LKB1 and CaMKKβ are essentialactivators of the AMPK signaling pathway. AMPK triggersproangiogenic effects through the eNOS protein in tissues withischemic conditions, where cells are vulnerable to apoptosis,autophagy and necrosis. The AMPK complex acts to restoreblood glucose levels and ATP levels back to homeostasis. Thisreview will discuss AMPK, as well as its key activators (LKB1and CaMKKβ), as a central energy regulator and evaluate theupstream and downstream regulating pathways of AMPK. Wewill also discuss how we can control this important enzyme inischemic conditions to prevent harmful effects in patients withvascular damage.
A Study on the Genetic Inheritance of Ankyloglossia Based on Pedigree Analysis
Soo-Hyung Han,Min-Cheol Kim1,Yun-Seok Choi,Jin-Soo Lim
Archives of Plastic Surgery , 2012, DOI: http://dx.doi.org/10.5999/aps.2012.39.4.329
Abstract: Background Ankyloglossia or tongue-tie is a congenital anomaly characterized by an abnormallyshort lingual frenum. Its prevalence in the newborn population is approximately 4%. Its modeof inheritance has been studied in some articles, but no conclusion has been established. Also,no relevant report has been published in Korea. This study was conducted to elucidate thegenetic inheritance of ankyloglossia via pedigree analysis.Methods In this study, 149 patients with no other congenital anomaly who underwentfrenuloplasty between March 2001 and March 2010 were studied. Pedigrees were made viapre- or post-operative history taking, and patients with uncertain histories were excluded.In the patient group that showed a hereditary nature, the male-to-female ratio, inheritancerate, and pattern of inheritance were investigated.Results One hundred (67.11%) of the patients were male and 49 (32.89%) were female(male-female ratio=2.04:1). Ninety-one (61.07%) patients reported no other relative withankyloglossia, and 58 (38.93%) patients had a relative with this disease. The inheritance ratewas 20.69% in the 58 cases with a hereditary nature. In the group with no family history ofankyloglossia, the male-female ratio was 3.79:1, which significantly differed from that ofthe group with a family history of ankyloglossia. X-chromosome mediated inheritance andvariation in the gene expression was revealed in the pedigree drawn for the groups withhereditary ankyloglossia.Conclusions Ankyloglossia has a significant hereditary nature. Our data suggest X-linkedinheritance. This study with 149 patients, the first in Korea, showed X-linked inheritance inpatients with a sole anomaly.
Angioleiomyoma of the Auricle
Hyo-In Kim1,Si-Gyun Roh1,Nae-Ho Lee1,Kyung-Moo Yang1
Archives of Plastic Surgery , 2013, DOI: http://dx.doi.org/10.5999/aps.2013.40.1.68
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