• Molecular & Cellular Toxicology
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• 제2권3호
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• pp.159-165
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• 2006

To determine the anticancer effect of D-amygdalin (D-mandelinitrole-${\beta}$-D-gentiobioside) in human chronic myeloid leukemia cells K562, we profiled the gene expression between amygdalin treatment and control groups. Through 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay, the cytotoxicity of D-amygdalin was $57.79{\pm}1.83%$ at the concentration of 5 mg/mL for 24 h. We performed cDNA microarray analysis and compared the gene expression profiles between D-amygdalin (5 mg/mL, 24 h) treatment and control groups. Among the genes changed by D-amygdalin, we paid attention to cell cycle-related genes, and particularly cell cycle regulator genes; because arrest of cell cycle processing was ideal tactic in remedy for cancer. In our data, expressions of cyclin-dependent kinase inhibitor 1B (p27, Kip1) (CDKN1B), ataxia telangiectasia mutated (includes complementation groups A, C, and D) (ATM), cyclin-dependent kinase inhibitor 1C (p57, Kip2) (CDKN1C), and CHK1 checkpoint homolog (CHEK1, formally known as CHK1) were increased, while expressions of cyclin-dependent kinase 2 (CDK2), cell division cycle 25A (CDC25A), and cyclin E1 (CCNE1) were decreased. The pattern of these gene expressions were confirmed through RT-PCR. Our results showed that D-amygdalin might control cell cycle regulator genes and arrest S phase of cell cycle in K562 cells as the useful anticancer drug.

• Archives of Plastic Surgery
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• 제34권6호
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• pp.671-678
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• 2007

Purpose: Venous malformation(VM) which often causes pain and discomfort is the most common type of vascular malformations. Although it is presented with disfigured appearance and associated soft tissue or skeletal hypertrophy, the molecular bases of VMs are poorly understood. Differentially expressed genes(DEGs) of VMs were investigated to illuminate the molecular mechanism of the disease entity. Methods: Gene expressions of VM patients' subcutaneous tissue were studied in comparison with normal persons' by $GeneFishing^{TM}$ technique using the annealing control primers (ACPs) to identify DEGs. Candidate genes were sequenced and screened by basic local alignment search tool (BLAST) afterwards. Results: Among seventy DEGs identified, forty DEGs which had shown significantly different expression pattern were sequenced. Twenty eight out of 40 were up-regulated while 12 were down-regulated. BLAST searches revealed that 37 were known genes and 3 were unknown genes. Many genes were involved in the differentiation and remodeling of smooth muscle cells, opposed to the previous hypothesis that a lot of angiogenetic genes would be involved. Furthermore, several transcription factors and related genes, as well as cell signaling and metabolism regulators, were up regulated. Conclusion: It suggests that analysis of DEGs in VMs provide basic knowledge about its pathophysiology. and new therapeutic approaches.

• Molecular & Cellular Toxicology
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• 제5권3호
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• pp.222-229
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• 2009

Our previous finding that pre-initiation treatment of indole-3-carbinol (I3C) represents a chemopreventive effect in dimethylbenz[a]anthracene (DMBA)-induced mammary carcinogenesis has prompted us to test the global expression of genes at an early stage. Rats were continuously fed 300 ppm I3C in their diet at 6 weeks of age and were injected with DMBA at 7 weeks of age, and were sacrificed at 8 weeks of age. Global gene expression analysis using oligonucleotide microarrays was conducted to detect altered genes in DMBA- or DMBA plus I3C-treated mammary glands. Altered genes were identified by fold changes of 1.2 and by t-test (P<0.05) from the log ratios of the hybridization intensity of samples between control (Group 1) and DMBA (Group 2), and from those of samples between DMBA (Group 2) and DMBA plus I3C (Group 3). From these genes, we chose altered genes that were up- or down-regulated by DMBA treatment and recovered to the control level by I3C treatment. For early stage of carcinogenesis, I3C treatment induced the recovery to normal levels of several genes including cell cycle pathway (cyclin B2, cell division cycle 2 homolog A), MAP signaling pathway (fibroblast growth factor receptor 1, platelet derived growth factor receptor, beta polypeptide), and insulin signaling (protein phosphatase 1, regulatory (inhibitor) subunit 3B and flotillin 2), which were up-regulated by DMBA treatment. In addition, I3C treatment induced the recovery to normal levels of several genes including those of MAPK signaling (transforming growth factor, beta receptor 1 and protein phosphatase 3, catalytic subunit, beta isoform), which were down-regulated by DMBA treatment. These results suggest that the targeting of these genes presents a possible approach for chemoprevention in DMBA-induced mammary carcinogenesis.

• BMB Reports
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• 제38권4호
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• pp.447-456
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• 2005

TNF-$\alpha$ plays a pivotal role in inflammation processes which are mainly regulated by endothelial cells. While TNF-$\alpha$ induces apoptosis of several cell types like tumor cells, endothelial cells are resistant to TNFa mediated cell death. The cytotoxic effects of TNF-$\alpha$ on most cells are only evident if RNA or protein synthesis is inhibited, suggesting that de novo RNA or protein synthesis protect cells from TNF-$\alpha$ cytotoxicity, presumably by NF-${\kappa}B$ mediated induction of protective genes. However, the cytoprotective genes involved in NF-${\kappa}B$ dependent endothelial cell survival have not been sufficiently identified. In the present study, the suppression subtractive hybridization (SSH) method was employed to identify rarely transcribed TNF-$\alpha$ inducible genes in human arterial endothelial cells related to cell survival and cell cycle. The TNF-$\alpha$-induced expression of the RNA binding protein $p54^{nrb}$ and the 14-3-3 protein HS1 as shown here for the first time may contribute to the TNF-$\alpha$ mediated cell protection of endothelial cells. These genes have been shown to play pivotal roles in cell survival and cell cycle control in different experimental settings. The concerted expression of these genes together with other genes related to cell protection and cell cycle like DnaJ, $p21^{cip1}$ and the ubiquitin activating enzyme E1 demonstrates the identification of new genes in the context of TNF-$\alpha$ induced gene expression patterns mediating the prosurvival effect of TNF-$\alpha$ in endothelial cells.

• Journal of Animal Science and Technology
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• 제54권3호
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• pp.157-163
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• 2012

The male reproduction is precisely controlled by a number of intrinsic and extrinsic factors. These factors usually involve in expressional regulation of various molecules influencing on sperm production in the testis. A number of ways are employed to control the transcription of specific genes, including epigenetic modifications of DNA and histone molecules. DNA methylation of CpG dinucleotides is a commonly used regulatory mechanism for testicular genes associated with the fertility. Previous studies have demonstrated the infertility induced by improper DNA methylation of these genes. In the present research, we attempted to determine transcriptional expression of some of these genes in the rat testis at different postnatal ages using real-time PCR analysis. These genes include neurotrophin 3 (Ntf3), insulin-like growth factor II (Igf2), JmjC-domain-containing histone demethylase 2A 1 (Jhm2da), paired box 8 transcription factor (Pax8), small nuclear ribonucleoprotein polypeptide N (Snrpn), and 5,10-methylenetetrahydrofolate reductase (Mthfr). The expression levels of Ntf3, Igf2, and Snrpn genes were the highest at the neonatal age, followed by transient decreases at the prepubertal age. Expression of Jhm2da and Mthfr genes were continuously increased from the neonate to 1 year of age. The levels of Pax8 mRNA at the early ages were higher than those at the later ages of postnatal development. These findings suggest that expression of some fertility-associated testicular genes in the rat during postnatal period could be differentially regulated by the control of the degree of DNA methylation.

• BMB Reports
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• 제36권1호
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• pp.28-34
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• 2003

Breast cancer is the most prevalent cancer among women in Western countries, and its prevalence is also increasing in Asia. The major risk factor for breast cancer can be traced to reproductive events that influence the lifetime levels of hormones. However, a large percentage of breast cancer cases cannot, be explained by these risk factors. The identification of susceptibility factors that predispose individuals to breast cancer (for instance, if they are exposed to particular environmental agents) could possibly give further insight into the etiology of this malignancy and provide targets for the future development of therapeutics. The most interesting candidate genes include those that mediate a range of functions. These include carcinogen metabolism, DNA repair, steroid hormone metabolism, signal transduction, and cell cycle control. We conducted a hospital-based case-control study in South Korea to evaluate the potential modifying role of the genetic polymorphisms of selected low penetrance genes that are involved in carcinogen metabolisms (i.e., CYP1A1, CYP2E1, GSTM1/T1/P1, NAT1/2, etc.), estrogen synthesis and metabolism (i.e., CYP19, CYP17, CYP1B1, COMT, ER-$\alpha$, etc.), DNA repair (i.e., XRCC1/3, ERCC2/4, ATM, AGT, etc.), and signal transduction as well as others (i.e., TGF-$\beta$, IGF-1, TNF-$\beta$, IL-1B, IL-1RN, etc.). We also took into account the potential interaction between these and the known risk factors of breast cancer. The results of selected genes will be presented in this mini-review.

• Journal of Veterinary Clinics
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• 제36권4호
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• pp.190-195
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• 2019

We aimed to identify genomic variations as well as the marker genes related with chronic mitral valve disease (CMVD) in Canis lupus familiaris using whole genome resequencing, which provides valuable resources for further study. Two ten-year old female Canis lupus familiaris English cocker spaniels were used for this study, one control and one who had been diagnosed as CMVD. For the whole genome resequencing, muscles from the left ventricular wall were collected from each dog. With the HiSeq DNA Shotgun library and $HiSeq^{TM}$ 2000 platform, whole genome resequencing was performed. From the results, we identified 5 million and 6 million variants in gene expression in the control and CMVD-diagnosed subject, respectively. We then selected the top 1,000 genes from the SNP, INS, and DEL mutation and 675 genes among them were overlapped for every mutation between the control and CMVD-diagnosed patient. Interestingly, in both groups, the intron variant (91.16 and 91.18%) and upstream variant (3.10 and 3.08%) are most highly related. Among the overlapped 675 genes, gene ontology for intracellular signal transduction is highly counted in INS, and DEL, and SNPs (35, 33, 31, respectively). In this study, we found that the COL and CDH gene families could be key molecules in identifying the difference in gene expression between control and CMVD-diagnosed dogs. We believe further studies will prove the importance of variants in key molecule expression and that these data will serve as a valuable foundation stone the study of canine CMVD.

• Korean Journal of Oriental Medicine
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• 제8권2호통권9호
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• pp.75-84
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• 2002

Obesity can be defined as a metabolic disease due to a increased state of fat tissue caused by an imbalance of calorie intake and use. To define genes that affected by different nutrient, we study gene expression from mice which were fed different nutrient. Epididymal and retro-peritineal adipose tissue were increase in high fat diet feeding mice compared with control, but liver and spleen were not. In serum, total cholesterol were differently increase in high fat diet feeding mice but total triglyceride and free fatty acid were not. That was maybe result of energy balance regulation in vivo system. aP2, PPART2 and FAS genes that were increased during adipogenesis were inclosed in high fat diet fed mice compared with control. In microarray assay, 1.4% of total genes were affected in epididymal adipose tissue by different nutrient. 1.1% of total genes were decreased down 0.5 fold and 0.3% were increased over 2 fold. These results indicated that many genes are affected in adipose tissue by nutrient.

• Research in Plant Disease
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• 제16권1호
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• pp.10-20
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• 2010

Root-knot nematodes cause billions of dollars in crop losses annually have a broad range of host over 2,000 species of plants. These nematodes are known as obligate, sedentary endo-parasites in a plant host to feed upon to complete their life cycle. To prevent the plant parasitic nematode, methyl bromide was widely applied as a soil fumigant. Other strategies to prevent or control nematodes involve RNAi-mediated suppression, R gene transformation, natural products or chemical treatments, the expression of peptide or proteins in susceptible plants, and others. Over the last decade, the entry in GenBank for Meloidogyne reveals 73,340 ESTs and recently two complete Meloidogyne spp. genomes sequences have simultaneously been presented by two groups. Recent works have demonstrated the effect of RNAi suppression to nematode target genes. These results will provide novel members of genes as a foundation for studies focused on understanding the function of M. incognita nematode genes as well as for the development of novel target genes for parasite control. Thus the successful development of biotechnology-derived plants with nematode resistance will result in large yield benefits for producers as well as environmental benefits and will accelerate the research related to pathogensresistant crops.

• Proceedings of the Korean Society of Crop Science Conference
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• 한국작물학회 2022년도 추계학술대회
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• pp.276-276
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• 2022

Wheat is one of the most widely grown food crops worldwide. Extreme precipitation and wind disturbances increased due to the abnormal climate, which resulted in increased lodging. Introduction of dwarf genes in wheat significantly increased lodging resistance and productivity in wheat breeding. In this study, we performed the genotyping of dwarfing genes between 'Keumkang' and 'Komac 5' ('Keumkang' mutant). In addition, we investigated the relationship between plant height and several phenotypic characters using F₂ segregation populations derived from crosses between the two varieties. There was no significant difference in phenotypic characters between the two varieties except for plant height. In the genotyping analysis using dwarfing genes, mutations of two dwarfing gene were found to be induced between the two varieties. The four genotypes of the F₂ populations from a crossing between 'Keumkang' and 'Komac 5' were used to compare and evaluate the effects of two dwarfing genes. Plants with two single mutant dwarfing gene and double mutant dwarfing gene revealed reduced plant heights than control plants by 4.5%, 6.9%, and 33.2%, respectively. The phenotype analysis showed that double mutant dwarfing gene affected wheat stem growth as the length decreases from the second node, resulting in decreased plant height. However, there were no significant differences in the agronomic traits between mutant plants and control plant. These results may provide novel information about the effect of double mutant dwarfing gene on plant height, and may help improve lodging tolerance and wheat yield.