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Won, Cheolhee,Lee, Chang Seok,Lee, Jin-Ku,Kim, Tack-Joong,Lee, Kwang-Ho,Yang, Young Mok,Kim, Yong-Nyun,Ye, Sang-Kyu,Chung, Myung-Hee Potamitis Press 2010 Anticancer research Vol.30 No.2
<P>The initiation and growth of hepatocellular carcinoma (HCC) are closely linked to chronic inflammation. Not only is cyclin D1 overexpressed, but it is also related to aggressive progression in HCC. However, the mechanism of expression cyclin D1, a cell-cycle regulator of paramount importance, in the tumor microenvironment remains unknown. Here, we investigated the mechanism of cyclin D1 expression induced by interleukin-6 (IL-6) and whether 3-[3,4-dihydroxy-phenyl]-acrylic acid 2-[3,4-dihydroxy-phenyl]-ethyl ester (CADPE), a derivate of caffeic acid, suppresses cyclin D1 expression. CADPE significantly inhibited IL-6-induced signal transducer and activator of transcription 3 (STAT3) activity in the Huh7 HCC cell line and attenuated IL-6-induced cyclin D1 transcription. Moreover, overexpression of constitutively active STAT3 increased cyclin D1 transcriptional activity and protein expression, whereas overexpression of a dominant-negative STAT3 deletion mutant (STAT3 (1-588)) reduced cyclin D1 transcriptional activity. In addition, CADPE effectively deacetylated histone 4 and prevented STAT3 recruitment to the cyclin D1 promoter, consistent with a role for the CADPE target, STAT3, in the regulation of cyclin D1 transcription. Collectively, these results indicate that CADPE suppresses cyclin D1 expression in HCC cells by blocking both IL-6-mediated STAT3 activation and recruitment of STAT3 to the cyclin D1 promoter.</P>
Won, Cheolhee,Kim, Byung‐,Hak,Yi, Eun Hee,Choi, Kyung‐,Ju,Kim, Eun‐,Kyung,Jeong, Jong‐,Min,Lee, Jae‐,Ho,Jang, Ja‐,June,Yoon, Jung‐,Hwan,Jeong, Won‐,Il,P John Wiley and Sons Inc. 2015 Hepatology Vol.62 No.4
<P>Enhanced expression of the cancer stem cell (CSC) marker, CD133, is closely associated with a higher rate of tumor formation and poor prognosis in hepatocellular carcinoma (HCC) patients. Despite its clinical significance, the molecular mechanism underlying the deregulation of CD133 during tumor progression remains to be clarified. Here, we report on a novel mechanism by which interleukin‐6/signal transducer and activator of transcription 3 (IL‐6/STAT3) signaling up‐regulates expression of CD133 and promotes HCC progression. STAT3 activated by IL‐6 rapidly bound to CD133 promoter and increased protein levels of CD133 in HCC cells. Reversely, in hypoxic conditions, RNA interference silencing of STAT3 resulted in decrease of CD133 levels, even in the presence of IL‐6, with a concomitant decrease of hypoxia‐inducible factor 1 alpha (HIF‐1α) expression. Active STAT3 interacted with nuclear factor kappa B (NF‐κB) p65 subunit to positively regulate the transcription of HIF‐1α providing a mechanistic explanation on how those three oncogenes work together to increase the activity of CD133 in a hypoxic liver microenvironment. Activation of STAT3 and its consequent induction of HIF‐1α and CD133 expression were not observed in Toll‐like receptor 4/IL‐6 double‐knockout mice. Long‐term silencing of CD133 by a lentiviral‐based approach inhibited cancer cell‐cycle progression and suppressed <I>in vivo</I> tumorigenicity by down‐regulating expression of cytokinesis‐related genes, such as TACC1, ACF7, and CKAP5. We also found that sorafenib and STAT3 inhibitor nifuroxazide inhibit HCC xenograft formation by blocking activation of STAT3 and expression of CD133 and HIF‐1α proteins. <I>Conclusion</I>: IL‐6/STAT3 signaling induces expression of CD133 through functional cooperation with NF‐κB and HIF‐1α during liver carcinogenesis. Targeting STAT3‐mediated CD133 up‐regulation may represent a novel, effective treatment by eradicating the liver tumor microenvironment. (H<SMALL>EPATOLOGY</SMALL> 2015;62:1160‐1173)</P>
Jae-Won Jang,Kyung-Eun Min,Cheolhee Kim,Jesik Shin,Jiwoon Lee,Sung Yi 한국정밀공학회 2023 International Journal of Precision Engineering and Vol.24 No.3
The goal of tissue engineering is to replace or regenerate damaged tissue. Scaffold fabrications and biomaterial selections are crucial factors for artificial tissue and bone tissue engineering, which are important due to the limited availability of tissue donors. This paper reviews the scaffold design considerations, manufacturing methods, and biomaterials for bone tissue engineering, and discusses current challenges and future perspectives. Scaffolds are required to have non-hazardous properties such as biocompatibility and biodegradability for the human body, and the necessary mechanical properties to support body weight, or to perform other roles, depending on the type of tissue. Moreover, scaffold structures such as porosity, pore size, and pore shape should be optimized to achieve cell viability and proliferation. Many conventional fabrication methods including thermally induced phase separation, emulsion freeze-drying, solvent casting, gas forming, and electrospinning have been studied and developed, but 3D printing is more suitable for bone tissue engineering because of its ability to manufacture complicated structures. Biomaterials can be divided into four categories: polymer, ceramic, metal, and composites. Composites blend two or more biomaterials to achieve desired properties for matching individual patient conditions. Finding a balance between fabrication method and biomaterial selection, in order to match properties between the scaffold and the target tissue, will be key to the field of bone tissue engineering in the future.
이철희(Cheolhee Lee),황태호(Taeho Hwang),원유집(Youjip Won),이성진(Seongjin Lee) Korean Institute of Information Scientists and Eng 2016 정보과학회논문지 Vol.43 No.7
Smart TV uses Webkit as a web browser engine to provide contents such as web surfing, VOD watching, and games. Webkit uses web resources, such as HTML, CSS, JavaScript, and images, in order to run applications. At the start of an application, Webkit loads resources to the memory and creates DOM tree and render tree, which is a time consuming process. However, DOM tree and render tree created by the smart TV application do not change over time because the smart TV application uses web resources stored in a disk. If DOM tree and render tree can be stored and reused, it is possible to reduce loading time of an application. In this paper, we propose FastIO technique that selectively adds persistency to dynamically allocated memory. FastIO reduces overall application loading time by eliminating the process of loading resources from storage, parsing the HTML documents, and creating DOM tree and render tree. Comparison of the application resource loading times indicates that the web browser with FastIO is 7.9x, 44.8x, and 2.9x faster than the legacy web browser in an SSD, Ramdisk, and eMMC environment, respectively.
Roh Sangho,Won Cheolhee,Min Byung-Moo 한국동물생명공학회(구 한국동물번식학회) 2005 Reproductive & Developmental Biology(Supplement) Vol.29 No.2s
This study was conducted to establish the optimal temperature condition before oocyte activation in B6D2 F1 mouse. In experiment 1, two embryo culture media (CZB vs KSOM) were evaluated for the development of activated mouse oocytes. Parthenogenetic embryos cultured in KSOM showed better blastocyst development than ones cultured in CZB(56.2% vs 81.0%, p<0.01). Two-hour of pre-incubation before activation significantly reduced the number of hatched blastocysts in KSOM (22.0% versus 8.8%, p<0.05). In experiment 2, recovered oocytes were pre-incubated at different temperature conditions before activation. The experimental groups were divided by 5 as follows. Group A: pre-incubation for 120 min at 37℃, Group B: pre-incubation at 37℃ for 90 min then at 25℃ for 30 min, Group C: pre-incubation at 37℃ for 60 min then at 25℃ for 60 min, Group D: pre-incubation at 37℃ for 30 min then at 25℃ for 90 min, and Group E: pre-incubation at 25℃ for 120 min before activation. Group A (67.6%) and B (66.7%) showed better development to the blastocyst stage than other groups (Group C: 50.0%, Group D: 49.2%, Group E: 33.3%, p<0.05). The present study indicates that the temperature before activation affects the development of B6D2 F1 mouse parthenogenetic oocytes and exposure to room temperature should be limited to 30-min when the oocytes are left in HEPES-buffered medium for micromanipulation.
PARK, Sang Kyu,WON, Cheolhee,CHOI, Young-Ju,KANG, Hoin,ROH, Sangho Japanese Society of Veterinary Science 2009 The Journal of veterinary medical science Vol.71 No.5
<P>Polarity formation in preimplantation embryos is controversial. To investigate the embryonic-abembryonic axis in the pig, porcine parthenotes were used to prevent the topological change caused by polyspermy as well as to avoid the influences of sperm entry position. For lineage tracing, DiI, a fluorescence dye, was injected into only a blastomere of the 2-cell stage embryos. If the first blastomere to divide was labeled, the embryo was included in the leading group, and while all others were included in the lagging group. In 60.5% of the blastocysts in the lagging group, the progeny of the labeled blastomeres formed the inner cell mass (ICM) and adjacent trophectoderm (TE) hemisphere; 62.1% of the blastocysts in the leading group had progeny of the labeled blastomeres distributed only to the TE (opposite of ICM). The rest of the lagging and leading groups showed random distributions. Unlike murine parthenotes, biased mitochondrial distribution was also found in porcine parthenotes (38.1%). Our findings indicate that the `leading' blastomere of the 2-cell porcine parthenote forms the distal TE (abembryonic) and that the `lagging' blastomere forms the remaining portion of the blastocyst, including the ICM (embryonic). Biased distribution of mitochondria in each 2-cell blastomere may contribute partly to this event.</P>
Lee, Chang Seok,Won, Cheolhee,Yoo, Hyouna,Yi, Eun Hee,Cho, Yuri,Maeng, Jung Woo,Sung, Sang Hyun,Ye, Sang-Kyu,Chung, Myung-Hee Pharmaceutical Society of Japan 2009 Biological & pharmaceutical bulletin Vol.32 No.11
<P>Fraxinellone and sauchinone, isolated from natural substance, are known to have an anti-inflammatory effect in inflammatory conditions. However, the anti-inflammatory actions of these compounds have been insufficiently demonstrated in viral-induced neuroinflammation. A viral component (double-stranded (ds)RNA) triggers a toll-like receptor 3-dependent inflammatory response that stimulates pro-inflammatory mediators in the brain. In present study, we initially examined the biological effects of fraxinellone and sauchinone on anti-inflammatory actions in dsRNA-stimulated microglia. Both compounds inhibited dsRNA-induced inducible nitric oxide synthase (iNOS) expression, a major pro-inflammatory enzyme. To demonstrate the mechanism of inhibitory effect on iNOS expression, we further examined the signaling pathway induced by dsRNA in microglia. Our data show that dsRNA promotes the expression of signal transducers and activators of transcription (STAT)1/3 identified as major inflammatory transcription factors as well as activates c-Jun N-terminal kinase (JNK) in an early time. Moreover, both compounds suppressed activation of JNK-STAT1/3 signaling pathway. These results suggest that an anti-inflammatory effect by fraxinellone and sauchinone is mediated <I>via</I> blockade of the JNK-STAT1/3-iNOS signaling pathway in viral-infected microglia.</P>