• Journal of Microbiology and Biotechnology
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• v.14 no.6
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• pp.1286-1294
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• 2004

In a previous study by the current authors, hepatocellular carcinoma (HCC) was determined to be epidemiologically sex-dependent, and the incidence and multiplicity of HCC found to decrease in estradiol-3 benzoate (EB)-treated F344 rats. Therefore, to ascertain the anticancer mechanism of EB, a commercially available cDNA microarray, with a total of 14,815 cDNA rat gene clones, was used to determine the differentially expressed genes in nontreated livers, EB-treated livers, and diethynitrosolamine (DEN)-induced HCC. In the sequenced experiment, a total of 85 genes were differentially expressed at either two or more times the rate of the normal expression, where 33 genes were downregulated by EB, and 52 genes upregulated. Candidate genes were selected according to significant changes observed in the mRNA expression in the EB-treated livers compared with the nontreated livers, then these genes were filtered according to their different expression patterns in the DEN-induced tumors compared to the estrogen-treated livers. To confirm the microarray data, a real-time PCR analysis was performed for ten selected genes: the H-ras revertant protein 107 (H­rev107), insulin-like growth factor binding protein (lOFBP), parathyroid hormone receptor (PI'HR), SH3 domain binding protein (SH3BP), metallothionein, src-suppressed C-kinase substrate (SSeCK) gene, phosphodiesterase I, CD44, epithelial membrane protein 3 (EMP3), and estrogen receptor a (ERa). The SSeCK and phosphodiesterase I genes were both upregulated in the DEN-induced hepatocarcinomas, yet their possible carcinogenic functions remain unknown. Meanwhile, the other genes were downregulated, including the genes related to growth regulation (IOFBP, H-revI07, ER$\alpha$), adipogenesis inhibition (PTHR), and tumor suppression (metallothionein).

• Journal of Radiation Industry
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• v.4 no.4
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• pp.325-334
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• 2010

Transcriptional regulation in response to salt in mutant lines was investigated using oligonucleotide microarrays. In order to characterize the salt-responsive genes in rice, the expression profiles of transcripts that responded to salt-treatment were monitored using the microarrays. In the microarray analysis, among 37,299 reliable genes, 5,101, 2,758 and 2,277 genes were up-regulated by more than 2-fold using the salt treatment, while the numbers of down-regulated genes were 4,619, 3,234, and 1,878 in the WT, ST-495, and ST-532, respectively. From genotype changes induced by gamma ray mutagenesis, 3,345 and 2,397 genes were up-regulated, while 2,745 and 2,075 genes were down-regulated more than 2-fold in the two untreated mutants lines compared with untreated WT, respectively. A total of 3,108 and 2,731 genes were up-regulated more than 2-fold, while 3,987 and 3,660 genes were down-regulated by more than 2-fold in the salt treatment of the two mutants lines compared with the salt treated WT, respectively. The expressions of membrane transporter genes such as OsAKT1, OsKUP, and OsNAC increased more severely in ST-495 and ST-532 than in the WT. The expressions of the proline accumulation related genes such as OsP5CS and OsP5CR were also markedly increased in the salt tolerant mutants when compared to the WT plant.

• Molecular & Cellular Toxicology
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• v.3 no.2
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• pp.90-97
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• 2007

8-Hydroxyquinoline is used as antibacterial agent and antioxidant based on its function inducing the chelation of ferrous ion present in host resulting in production of chelated complex. This complex being transported to cell membrane of bacteria and fungi exerts antibacterial and antifungal action. In this study, we have carried out in vitro genetic toxicity tests and microarray analysis to understand the underlying mechanisms and the mode of action of toxicity of 8-hydroxyquinoline. TA1535 and TA98 cells were treated with 8-hydroxyquinoline to test its toxicity by basic genetic toxicity test, Ames and two new in vitro micronucleus and COMET assays were applied using CHO cells and L5178Y cells, respectively. In addition, microarray analysis of differentially expressed genes in L5178Y cells in response to 8-hydroxyquinoline were analyzed using Affymatrix genechip. The result of Ames test was that 8-hydroxyquinoline treatment increased the mutations in base substitution strain TA1535 and likewise, 8-hydroxyquinoline also increased mutations in frame shift TA98. 8-Hydroxyquinoline increased micronuclei in CHO cells and DNA damage in L5178Y. 8-Hdroxyquinoline resulted in positive response in all three tests showing its ability to induce not only mutation but also DNA damage. 783 Genes were initially selected as differentially expressed genes in response to 8-hydroxyquinoline by microarray analysis and 34 genes among them were over 4 times of log fold changed. These 34 genes could be candidate biomarkers of genetic toxic action of 8-hydroxyquinoline related to induction of mutation and/or induction of micronuclei and DNA damage. Further confirmation of these candidate markers related to their biological function will be useful to understand the detailed mode of action of 8-hydroxyquinoline.

• Radiation Oncology Journal
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• v.21 no.1
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• pp.54-65
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• 2003

Purpose : To analyze the gene expression Profiles of uterine ceulcal cancer, and its variation after radiation therapy, with or without concurrent chemotherapy, using a CDNA microarray. Materials and Methods :Sixteen patients, 8 with squamous ceil carcinomas of the uterine cervix, who were treated with radiation alone, and the other 8 treated w14h concurrent chemo-radiation, were Included in the study. Before the starling of the treatment, tumor biopsies were carried out, and the second time biopsies were peformed after a radiation dose of 16.2$\~$27 Gy. Three normal cervix tissues were used as a control group. The microarray experiments were peformed with 5 groups of the total RNAs extracted individually and then admixed as control, pre-radiation therapy alone, during-radiation therapy alone, pre-chemoradiation therapy, and during-chemoradlation therapy. The 33P-iabeled CDNAS were synthesized from the total RNAs of each group, by reverse transcription, and then they were hybridized to the CDNA microarray membrane. The gene expression of each microarrays was captured by the intensity of each spot produced by the radioactive isotopes. The pixels per spot were counted with an Arrayguage, and were exported to Microsoft Excel The data were normalized by the Z transformation, and the comparisons were peformed on the Z-ratio values calculated. Results : The expressions of 15 genes, including integrin linked kinase (ILK), CDC28 protein kinase 2, Spry 2, and ERK 3, were increased with the Z-ratio values of over 2.0 for the cervix cancer tissues compared to those for the normal controls. Those genes were involved In cell growth and proliferation, cell cycle control, or signal transduction. The expressions of the other 6 genes, Including G protein coupled receptor kinase 5, were decreased with the Z-ratio values of below -2.0. After the radiation thorapy, most of the genes, with a previously Increase expressions, represented the decreased expression profiles, and the genes, with the Z-ratio values of over 2.0, were cyclic nucleotlde gated channel and 3 Expressed sequence tags (EST). In the concurrent chemo-radiation group, the genes involved in cell growth and proliferation, cell cycle control, and signal transduction were shown to have increased expressions compared to the radiation therapy alone group. The expressions of genes involved in anglogenesis (angiopoietln-2), immune reactions (formyl peptide receptor-iike 1), and DNA repair (CAMP phosphodiesterase) were increased, however, the expression of gene involved In apoptosls (death associated protein kinase) was decreased. Conclusion : The different kinds of genes involved in the development and progression of cervical cancer were identified with the CDNA microarray, and the proposed theory is that the proliferation signal stalls with ILK, and is amplified with Spry 2 and MAPK signaling, and the cellular mitoses are Increased with the increased expression oi Cdc 2 and cell division kinases. After the radiation therapy, the expression profiles demonstrated 4he evidence of the decreased cancer cell proliferation. There was no sigificant difference in the morphological findings of cell death between the radiation therapy aione and the chemo-radiation groups In the second time biopsy specimen, however, the gene expression profiles were markedly different, and the mechanism at the molecular level needs further study.

• BMB Reports
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• v.50 no.8
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• pp.411-416
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• 2017

The endoplasmic reticulum (ER) membrane protein complex subunit 6 (EMC6) is a novel human autophagy-related molecule. Here, using tissue microarray and immunohistochemistry, we report that EMC6 protein is lost or reduced in glandular cells of patients with gastric adenocarcinoma, compared to normal stomach mucosa. Overexpression of EMC6 in gastric cancer cells inhibited cell growth, migration, invasion, and induced apoptosis and cell cycle arrest at S-phase. Further investigation suggested that EMC6 overexpression in BGC823 human adenocarcinoma gastric cancer cells reduced tumorigenicity in a xenograft model, demonstrating that EMC6 has the characteristics of a tumor suppressor. This is the first study to show that EMC6 induces cell death in gastric cancer cells. The molecular mechanism of how EMC6 functions as a tumor suppressor needs to be further explored.

• Journal of Yeungnam Medical Science
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• v.37 no.2
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• pp.73-78
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• 2020

Cancer incidence has been increasing steadily and is the leading cause of mortality worldwide. Gastric cancer is still most common malignancy in Korea. Cancer initiation and progression are multistep processes involving various growth factors and their ligands. Among these growth factors, we have studied hepatocyte growth factor (HGF), which is associated with cell proliferation and invasion, leading to cancer and metastasis, especially in gastric cancer. We explored the intercellular communication between HGF and other surface membrane receptors in gastric cancer cell lines. Using complimentary deoxyribonucleic acid microarray technology, we found new genes associated with HGF in the stomach cancer cell lines, NUGC-3 and MKN-28, and identified their function within the HGF pathway. The HGF/N-methyl-N'-nitroso-guanidine human osteosarcoma transforming gene (c-MET) axis interacts with several molecules including E-cadherin, urokinase plasminogen activator, KiSS-1, Jun B, and lipocalin-2. This pathway may affect cell invasion and metastasis or cell apoptosis and is therefore associated with tumorigenesis and metastasis in gastric cancer.

• Animal cells and systems
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• v.7 no.1
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• pp.89-92
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• 2003

Immunoassays have become indispensable tools and achieved great importance in scientific and medical research. However, typical immunoassays are time-consuming and use complex, multi-step procedures. In this study, we introduce a new immunoassay system for the quantification of several analytes at a time without any washing steps. It is comprised of a detector solution with fluorescence-labeled antibodies and a test strip with immobilized capture antibodies. Using a micro-array scanner, the antigen-antibody complex was quantitatively determined by measuring the intensities of fluorescence on the capture lines or dots of nitrocellulose membrane. This method demonstrated its rapid quantitative determination of analytes without many processing steps as well as specific identification of multiple analytes in biological specimens.

• Proceedings of the Korean Society for Applied Microbiology Conference
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• 2003.06a
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• pp.129-131
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• 2003

Recombinant bioluminescent bacteria and cultured human cells were applied for toxicogenomic analysis of environmentally hazardous chemicals. Recombinant bioluminescent biosensing cells were used to detect and classify the toxicity caused by various chemicals. Classification of toxicity was realized based upon the chemicals' mode of action using DNA-, oxidative-, protein, and membrane-damage sensitive strains. As well, a simple double-layered cell culture system using Caco-2 cells and Hep G2 cells, which mimic the metabolic processes occurring in humans, such as adsorption through the small intestine and biotransformationin both the small intestine and the liver, was developed to investigate the toxicity of hazardous materials to humans. For a more in-depth analysis, a DNA microarray was used to study the transcriptional responses of Caco-2 and Hep G2 cells to benzo〔a〕pyrene.

• Journal of Physiology & Pathology in Korean Medicine
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• v.21 no.5
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• pp.1285-1290
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• 2007

The present study aims to identify and characterize genes that cause differen genes between non-responders and responders to electroacupuncture (EA) on mechanical allodynia following peripheral nerve injury. Under sodium pentobarbital anesthesia, animals were subjected to unilateral transection of the superior caudal trunk at the level between S1 and S2 spinal nerves. EA stimulation (2Hz, 0.3 ms, 0.2-0.3 mA) was delivered to Zusanli (ST36) for 30 min 2 weeks after the surgery. The degree of mechanical allodynia was assessed quantitatively by touching the tail with von Frey hair (2.0 g) at 10 min intervals. The rats, which showed an EA-induced decrease of response frequencies under 10 %, were classified as non-responders and those displaying an EA-induced decrease of response frequencies 20 % or more were classified as responders. Results from oligonucleotide microarray, to which cDNAs from the spinal dorsal horn (DH) were applied, showed that hemoglobin beta chain complex and chondroitin sulfate proteoglycan-5 decreased and limbic system-associated membrane protein increased in the non-responder group, whereas calcium-independent alpha-Iatrotoxin receptor homolog-3 increased in the responder group. These results suggest that The functional abnormality of molecules regulating cell adhesion, intracellular signal transduction and cell differentiation in the spinal DH may be involved in the anti-allodynic effect of EA.

• Journal of Applied Biological Chemistry
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• v.58 no.3
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• pp.227-232
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• 2015

A microarray study has been employed to understand changes of gene expression in E. coli KD43162 resistant to ampicillin, ampicillin-sulbactam, piperacillin, piperacillin-tazobactam, cefazolin, cefepime, aztreonam, imipenem, meropenem, gentamicin, tobramycin, ciprofloxacin, levofloxacin, moxifloxacin, fosfomycin, and trimethoprim-sulfamethoxazole except for amikacin using disk diffusion assay. Using Sodium dodecyl sulphate-polyacrylamide gel electrophoresis and MALDI-TOF MS analyses, 36 kDa of outer membrane proteins (OMPs) was found to be deleted in the multidrug resistant E. coli KD 43162. Microarray analysis was used to determine up- and down-regulated genes in relation to multidrug resistant E. coli KD43162. Among the up-regulated genes, these genes were corresponded to express the proteins as penicillin-binding proteins (PBPs), tartronate semialdehyde reductase, ethanolamine utilization protein, shikimate kinase I, allantoinase, predicted SAM-dependent methyltransferase, L-glutamine: D-fructose-6-phosphate aminotransferase (GFAT), phospho-glucosamine mutase, predicted N-acetylmannosamine kinase, and predicted N-acetylmannosamine-6-P epimerase. Up-regulation of PBPs, one of primary target sites of antibiotics, might be responsible for the multidrug resistance in E. coli with increasing amount of target sites. Up-regulation of GFAT enzyme may be related to the up-regulation of PBPs because GFAT produces N-acetylglucosamine, a precursor of peptidoglycans. One of GFAT inhibitors, azaserine, showed a potent inhibition on the growth of E. coli KD43162. In conclusion, up-regulation of PBPs and GFATs with the loss of 36 kDa OMP refers the multidrug resistance in E. coli KD 43162.