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Search Results: 1 - 10 of 6936 matches for " Cheol-Hee Choi "
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ABC transporters as multidrug resistance mechanisms and the development of chemosensitizers for their reversal
Cheol-Hee Choi
Cancer Cell International , 2005, DOI: 10.1186/1475-2867-5-30
Abstract: One of the major problems related with anticancer chemotherapy is resistance against anticancer drugs. Some cancers such as non-small cancer, lung cancer, and rectal cancer show what is called primary resistance or natural resistance in which they do not respond to standard chemotherapy drugs from the beginning. On the other hand, many types of sensitive tumors respond well to chemotherapy drugs in the beginning but show acquired resistance later. Experimentally, drug resistance could be very specific to the drug used due to abnormal genetic machinery such as gene amplification within tumor cells in many cases. Multidrug resistance (MDR) is especially problematic in acquired drug resistance. MDR is the phenomenon in which cancer cells exposed to one anticancer drug show resistance to various anticancer drugs that are structurally and functionally different from the initial anticancer drug. The most investigated mechanisms with known clinical significance are: a) activation of transmembrane proteins effluxing different chemical substances from the cells; b) activation of the enzymes of the glutathione detoxification system; c) alterations of the genes and the proteins involved into the control of apoptosis (especially p53 and Bcl-2). The cell membrane, cytoplasm, and nuclear protein participate in these resistance mechanisms [1]. The resistance mechanism is called typical MDR or classical MDR when overexpression of the membrane efflux pumps is involved in MDR. The classical MDR is due mostly to increased efflux pumps in the cell membrane of cells pumping anticancer drugs out of cells. The most typical efflux pumps in the cell membrane is P-glycoprotein (Pgp) [2] having the molecular weight of 170 KD, due to the gene amplification of the normal human gene, MDR1. The efflux pump Pgp is responsible for transporting various xenobiotics (not limited to anticancer drugs) out of cells by using ATP (Fig. 1) [3]. Pgp is one of the membrane transporter superfamily having the A
Epigenetic mechanisms involved in differential MDR1 mRNA expression between gastric and colon cancer cell lines and rationales for clinical chemotherapy
Tae-Bum Lee, Jung-Hee Park, Young-Don Min, Kyung-Jong Kim, Cheol-Hee Choi
BMC Gastroenterology , 2008, DOI: 10.1186/1471-230x-8-33
Abstract: The MDR1 mRNA levels were determined using PCR and real-time PCR assays after reverse transcription. Cytotoxicity was performed using the MTT assay. Methylation status was explored by quantification PCR-based methylation and bisulfite DNA sequencing analyses.The MDR1 mRNA levels obtained by 35 cycles of RT-PCR in gastric cancer cells were just comparable to those obtained by 22 cycles of RT-PCR in colon cancer cells. Real-time RT-PCR analysis revealed that MDR1 mRNA was not detected in the 10 gastric cancer cell lines but variable MDR1 mRNA levels in 7 of 9 colon cancer cell lines except the SNU-C5 and HT-29 cells. MTT assay showed that Pgp inhibitors such as cyclosporine A, verapamil and PSC833 sensitized Colo320HSR (colon, highest MDR1 expression) but not SNU-668 (gastric, highest) and SNU-C5 (gastric, no expression) to paclitaxel. Quantification PCR-based methylation analysis revealed that 90% of gastric cancer cells, and 33% of colon cancer cells were methylated, which were completely matched with the results obtained by bisulfite DNA sequencing analysis. 5-aza-2'-deoxcytidine (5AC, a DNA methyltransferase inhibitor) increased the MDR1 mRNA levels in 60% of gastric cells, and in 11% of colon cancer cells. Trichostatin A (TSA, histone deacetylase inhibitor) increased the MDR1 mRNA levels in 70% of gastric cancer cells and 55% of colon cancer cells. The combined treatment of 5AC with TSA increased the MDR1 mRNA levels additively in 20% of gastric cancer cells, but synergistically in 40% of gastric and 11% of colon cancer cells.These results indicate that the MDR1 mRNA levels in gastric cancer cells are significantly lower than those in colon cancer cells, which is at least in part due to different epigenetic regulations such as DNA methylation and/or histone deacetylation. These results can provide a better understanding of the efficacy of combined chemotherapy as well as their oral bioavailability.Gastric and colorectal cancers are a cause of morbidity and mortal
Functional and structural characteristics of anticancer peptide Pep27 analogues
Dong Lee, Kyung-Soo Hahm, Yoonkyung Park, Hai-Young Kim, Weontae Lee, Sung-Chul Lim, Youn-Kyung Seo, Cheol-Hee Choi
Cancer Cell International , 2005, DOI: 10.1186/1475-2867-5-21
Abstract: Pep27anal2 characterized substituting (2R→W), (4E→W), (11S→W) and (13Q→W) in native Pep27, exhibited greater hydrophobicity and anticancer activity than Pep27 and other analogues. The IC50 values of Pep27anal2 were approximately 10 – 30 μM in a number of cell lines (AML-2, HL-60, Jurkat, MCF-7 and SNU-601). Confocal microscopy showed that Pep27anal2-FITC was localized in the plasma membrane, and then moving from the membrane to subcellular compartments with the initiation of membrane blebbing. Flow cytometric analysis using propidium iodide and Annexin V also revealed that Pep27anal2 induced apoptosis with minor membrane damage. Electron microscopy revealed that Pep27 induced apoptosis in Jurkat cells. The anticancer activity of Pep27anal2 was neither abrogated by pan-caspase inhibitor (Z-VAD-fmk) nor related to cytochrome c release from mitochondria. The 3D solution structures of these two Pep27 peptides revealed that both form a random coil conformation in water; however, they adopted stable α-helical conformations in solutions.The results indicate that Pep27anal2 can penetrate the plasma membrane, and then induce apoptosis in both caspase-and cytochrome c-independent manner. The hydrophobicity of Pep27anal2 appears to play an important role in membrane permeabilization and/or anticancer properties. The structure-functional relationships of these peptides are also discussed. It is proposed that Pep27anal2 is a potential candidate for anticancer therapeutic agents.Newly discovered peptides are becoming increasingly important, not only as molecular tools for the understanding of protein-protein interactions, but also as lead compounds. Cationic amphipathic peptides, such as cecropins, defensins, and mellitin, induce cell death in prokaryotic and eukaryotic cells by increasing membrane permeability [1]. This increased permeability may lead to cell lysis or, alternatively, may produce subtle changes in the membrane barrier function and promote cell death [2]. It has a
Distributed Intelligent Microgrid Control Using Multi-Agent Systems  [PDF]
Il-Yop Chung, Cheol-Hee Yoo, Sang-Jin Oh
Engineering (ENG) , 2013, DOI: 10.4236/eng.2013.51B001
Abstract: In the future, the individual entities of microgrids such as distributed generators and smart loads may need to determine their power generation or consumption in more economic ways. Intelligent agents can help the decision-making procedure of the entities by intelligent algorithms and state-of-the-art communication with central controller and other local agents. This paper presents the development of atable-top microgrid control system using multi-agent systems and also the demonstration of demand response programs during power shortage. In our table-top system, agents are implemented using microcontrollers and Zigbee wireless communication technology is applied for efficient data communication in the multi-agent system. The power system models of distributed generators and loads are implemented in the real-time simulator using Opal-RT system. The whole test system that includes real-time system simulation and agent hardware is implemented in the hardware-in-the-loop simulation framework. The performance of the developed system is tested for emergency demand response cases.
Molecular mechanisms of heptaplatin effective against cisplatin-resistant cancer cell lines: less involvement of metallothionein
Cheol-Hee Choi, Yoon-Jung Cha, Chun-San An, Kyung-Jong Kim, Kweon-Cheon Kim, Sung-Pyo Moon, Zang Lee, Young-Don Min
Cancer Cell International , 2004, DOI: 10.1186/1475-2867-4-6
Abstract: Molecular mechanisms of heptaplatin effective against cisplatin-resistant cancer cell lines has been investigated in connection with metallothionein (MT). Cytotoxicity was determined by an MTT assay. MT mRNA, was determined by RT-PCR assay. Transfection study was carried out to examine the function of MT.Of various gastric cancer cell lines, SNU-638 and SNU-601 showed the highest and lowest levels of MT mRNA, respectively, showing 80-fold difference. The IC50 values of SNU-638 to cisplatin, carboplatin and heptaplatin were 11.2-fold, 5.1-fold and 2.0-fold greater than those of SNU-601, respectively. Heptaplatin was more effective against cisplatin-resistant and MT-transfected gastric cancer sublines than cisplatin or carboplatin was. In addition, heptaplatin attenuated cadmium, but not zinc, induction of MT.These results indicate that molecular mechanisms of heptaplatin effective against cisplatin-resistant gastric cancer sublines is at least in part due to the less involvement of MT in heptaplatin resistance as well as its attenuation of MT induction.Gastric cancer is the most frequently diagnosed and the second leading cause of cancer-related death in Korea. For many years, a few single agents such as 5-fluorouracil, doxorubicin, mitomycin C, and nitrosourea, have been considered to have significant antitumor activity in gastric cancer patients [1]. However, the response rate has been <30% and complete remission has been rare. Several combination chemotherapy regimens such as FAM (5-fluorouracil, adriamycin, and mitomycin C) have been attempted in order to improve the treatment outcomes. In a nonrandomized Phase II study for advanced gastric cancer, the FAM regimen achieved an objective partial response rate of 42% [2]. Some cisplatin-based combination chemotherapy regimens have shown high response rates [3,4].Despite the efficacy of cisplatin against gastric cancer, there were two major problems with this agent. Firstly, there are significant side effects, such a
Hardware-in-the-Loop Simulation of Distributed Intelligent Energy Management System for Microgrids
Sang-Jin Oh,Cheol-Hee Yoo,Il-Yop Chung,Dong-Jun Won
Energies , 2013, DOI: 10.3390/en6073263
Abstract: Microgrids are autonomous low-voltage power distribution systems that contain multiple distributed energy resources (DERs) and smart loads that can provide power system operation flexibility. To effectively control and coordinate multiple DERs and loads of microgrids, this paper proposes a distributed intelligent management system that employs a multi-agent-based control system so that delicate decision-making functions can be distributed to local intelligent agents. This paper presents the development of a hardware-in-the-loop simulation (HILS) system for distributed intelligent management system for microgrids and its promising application to an emergency demand response program. In the developed HILS system, intelligent agents are developed using microcontrollers and ZigBee wireless communication technology. Power system dynamic models are implemented in real-time simulation environments using the Opal-RT system. This paper presents key features of the data communication and management schemes based on multi-agent concepts. The performance of the developed system is tested for emergency demand response program applications.
Intelligent Control of Battery Energy Storage for Multi-Agent Based Microgrid Energy Management
Cheol-Hee Yoo,Il-Yop Chung,Hak-Ju Lee,Sung-Soo Hong
Energies , 2013, DOI: 10.3390/en6104956
Abstract: Microgrids can be considered as controllable units from the utility point of view because the entities of microgrids such as distributed energy resources and controllable loads can effectively control the amount of power consumption or generation. Therefore, microgrids can make various contracts with utility companies such as demand response program or ancillary services. Another advantage of microgrids is to integrate renewable energy resources to low-voltage distribution networks. Battery energy storage systems (BESSs) can effectively compensate the intermittent output of renewable energy resources. This paper presents intelligent control schemes for BESSs and autonomous energy management schemes of microgrids based on the concept of multi-agent systems. The proposed control scheme consists of two layers of decision-making procedures. In the bottom layer, intelligent agents decide the optimal operation strategies of individual microgrid entities such as BESSs, backup generators and loads. In the upper layer, the central microgrid coordinator (MGCC) coordinates multiple agents so that the overall microgrid can match the load reduction requested by the grid operator. The proposed control scheme is applied to Korea Power Exchange’s Intelligent Demand Response Program.
Crucial Role of TSC-22 in Preventing the Proteasomal Degradation of p53 in Cervical Cancer
Cheol-Hee Yoon, Seung Bae Rho, Seong-Tae Kim, Seongho Kho, Junsoo Park, Ik-Soon Jang, Seonock Woo, Sung Soon Kim, Je-Ho Lee, Seung-Hoon Lee
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0042006
Abstract: The p53 tumor suppressor function can be compromised in many tumors by the cellular antagonist HDM2 and human papillomavirus oncogene E6 that induce p53 degradation. Restoration of p53 activity has strong therapeutic potential. Here, we identified TSC-22 as a novel p53-interacting protein and show its novel function as a positive regulator of p53. We found that TSC-22 level was significantly down-regulated in cervical cancer tissues. Moreover, over-expression of TSC-22 was sufficient to inhibit cell proliferation, promote cellular apoptosis in cervical cancer cells and suppress growth of xenograft tumors in mice. Expression of also TSC-22 enhanced the protein level of p53 by protecting it from poly-ubiquitination. When bound to the motif between amino acids 100 and 200 of p53, TSC-22 inhibited the HDM2- and E6-mediated p53 poly-ubiquitination and degradation. Consequently, ectopic over-expression of TSC-22 activated the function of p53, followed by increased expression of p21Waf1/Cip1 and PUMA in human cervical cancer cell lines. Interestingly, TSC-22 did not affect the interaction between p53 and HDM2. Knock-down of TSC-22 by small interfering RNA clearly enhanced the poly-ubiquitination of p53, leading to the degradation of p53. These results suggest that TSC-22 acts as a tumor suppressor by safeguarding p53 from poly-ubiquitination mediated-degradation.
An Obligatory Role of Mind Bomb-1 in Notch Signaling of Mammalian Development
Bon-Kyoung Koo, Mi-Jeong Yoon, Ki-Jun Yoon, Sun-Kyoung Im, Yoon-Young Kim, Cheol-Hee Kim, Pann-Ghill Suh, Yuh Nung Jan, Young-Yun Kong
PLOS ONE , 2007, DOI: 10.1371/journal.pone.0001221
Abstract: Background The Notch signaling pathway is an evolutionarily conserved intercellular signaling module essential for cell fate specification that requires endocytosis of Notch ligands. Structurally distinct E3 ubiquitin ligases, Neuralized (Neur) and Mind bomb (Mib), cooperatively regulate the endocytosis of Notch ligands in Drosophila. However, the respective roles of the mammalian E3 ubiquitin ligases, Neur1, Neur2, Mib1, and Mib2, in mammalian development are poorly understood. Methodology/Principal Findings Through extensive use of mammalian genetics, here we show that Neur1 and Neur2 double mutants and Mib2?/? mice were viable and grossly normal. In contrast, conditional inactivation of Mib1 in various tissues revealed the representative Notch phenotypes: defects of arterial specification as deltalike4 mutants, abnormal cerebellum and skin development as jagged1 conditional mutants, and syndactylism as jagged2 mutants. Conclusions/Significance Our data provide the first evidence that Mib1 is essential for Jagged as well as Deltalike ligand-mediated Notch signaling in mammalian development, while Neur1, Neur2, and Mib2 are dispensable.
Cug2 is essential for normal mitotic control and CNS development in zebrafish
Hyun-Taek Kim, Ju-Hoon So, Seung-Hyun Jung, Dae-Gwon Ahn, Wansoo Koh, Nam-Soon Kim, Soo-Hyun Kim, Soojin Lee, Cheol-Hee Kim
BMC Developmental Biology , 2011, DOI: 10.1186/1471-213x-11-49
Abstract: To study the function of CUG2 in vivo, we isolated a zebrafish homologue that is expressed specifically in the proliferating cells of the central nervous system (CNS). Morpholino-mediated knockdown of cug2 resulted in apoptosis throughout the CNS and the development of neurodegenerative phenotypes. In addition, cug2-deficient embryos contained mitotically arrested cells displaying abnormal spindle formation and chromosome misalignment in the neural plate.Therefore, our findings suggest that Cug2 is required for normal mitosis during early neurogenesis and has functions in neuronal cell maintenance, thus demonstrating that the cug2 deficient embryos may provide a model system for human neurodegenerative disorders.Cancer-upregulated gene 2 (CUG2) is known to be differentially expressed in multiple human cancer tissues including the ovary, liver, lung, intestines and pancreas [1]. Mammalian cells overexpressing CUG2 showed hallmarks of neoplasmic transformation in vitro, such as increased cell proliferation, migration, invasion, anchorage-independent growth and tumor formation in nude mice, similar to the effects of the H-ras oncogene [1].Recently, CUG2 was shown to interact with CENP-T and CENP-A, essential components of the nucleosome complex located at the centromere, and was hence named centromere protein W (CENP-W) [2,3]. The centromere is involved in sister chromatid cohesion and the attachment of spindle microtubules, and is thus responsible for accurate chromosome segregation during mitotic and meiotic cell division [4]. CENP-A, a histone H3-like core protein, is required for the recruitment of many constitutive centromere components as well as transient kinetochore components [5,6]. We and others have reported that CUG2/CENP-W forms a DNA-binding complex together with the CENP-T and CENP-A as part of the centromere chromatin structure [2,3]. SiRNA-mediated knockdown of CUG2/CENP-W in HeLa cells caused defective mitosis characterized by multipolar spindle forma
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