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Jung, Samil,Yi, Lisha,Jeong, Dongjun,Kim, Jinsun,An, Sungwhan,Oh, Tae-Jeong,Kim, Chang-Hwan,Kim, Chang-Jin,Yang, Young,Kim, Keun Il,Lim, Jong-Seok,Lee, Myeong-Sok National Hellenic Research Foundation 2011 ONCOLOGY REPORTS Vol.25 No.1
<P>The ADCYAP1 gene encodes an adenylate cyclase activating polypeptide 1. ADCYAP1 has been known to be involved in various biological processes. Multiple cytosine guanine dinucleotides (CpG island) are found in the ADCYAP1 promoter region. Transcriptional silencing by promoter hypermethylation is an important regulatory mechanism in tumorigenesis in many cancers. Therefore, the methylation level of the ADCYAP1 promoter was investigated in eight cervical cancer cell lines and human tissue samples with a distinctive degree of malignant transformation. While multiple CpG sites in the ADCYAP1 promoter were highly methylated in CIN III and invasive carcinoma cells as well as seven cervical cancer cell lines, they were rarely methylated in normal cells. Importantly, methylation in the ADCYAP1 promoter seems to start from CIN I, relatively early stage of multistep carcinogenesis. This fact suggest that ADCYAP1 can be used as an effective and sensitive methylation biomarker for the early diagnosis of cervical cancer. Moreover, our data imply that the level of the ADCYAP1 promoter hypermethylation is correlated with cervical cancer development. We also show that ADCYAP1 gene expression was reactivated by the treatment of a DNA methyltransferase inhibitor of 5'-aza-2'deoxycytidine and/or a histone deacetylase inhibitor of trichostain A in cervical cancer cells suggesting that hypermethylation in the ADCYAP1 promoter is responsible for the transcriptional silencing of the ADCYAP1 gene in cervical cancer cells.</P>
Epigenetic regulation of the potential tumor suppressor gene, hLHX6.1, in human cervical cancer
JUNG, SAMIL;JEONG, DONGJUN;KIM, JINSUN;YI, LISHA;KOO, KEUNHOE;LEE, JAEHYOUK;KIM, CHANG-JIN;KIM, CHANG-HWAN;AN, SUNGWHAN;YANG, YOUNG;LIM, JONG-SEOK;KIM, KEUN IL;LEE, MYEONG-SOK Sookmyung Women's University Research Institute of 2011 여성과 건강 Vol.6 No.2
It is well known that the Homo sapiens LIM homeobox domain 6 gene (hLHX6), a putative transcription regulator, controls the differentiation and development of neural and lymphoid cells, particularly in the central nervous system. In this study, we investigated hLHX6.1 (an isoform of hLHX6), which functions as a tumor suppressor gene in the cervix. Firstly, the methylation levels of the h내X6 and hLHX6.1 promoters were investigated in 8 cervical cancer cell lines and human tissue samples with a distinctive degree of malignant transformation. In spite of the presence of multiple cytosine guanine dinucleotides (CpG islands) in 2 proximal promoters of the hLHX6 and hLHX6.1 genes, only the HLHX6.1 promoters were found to be mostly hyper¬methylated and associated with transcriptional silencing by promoter methylation, whereas the hLHX6 promoters were not. Methylation levels in the hLX6.1 promoter were also found to be strongly related to cervical cancer development. The level of hLHX6.1 gene expression was found to be relatively high in normal cells, in which the hLHX6.1 promoter was mostly unmethylated. However, the hLHX6.1 gene expression was down-regulated or undetectable in cervical cancer cell lines and cancer tissues, in which the hLHX6.1 promoter was hypermethylated. This epigenetic alteration in the hLHX6.1 promoter begins at a relatively early stage, suggesting its potential as a biomarker for the early diagnosis and prevention of cervical cancer. Moreover, the overexpression of the hLHX6.1 gene in cervical cancer cells suppressed the tumorigenic phenotype, as shown by soft agar colony formation and migration assays, suggesting that hLHX6.1 could be a new tumor suppressor gene in the cervix.
JUNG, SAMIL;YI, LISHA;JEONG, DONGJUN;KIM, JINSUN;AN, SUNGWHAN;OH, TAE-JEONG;KM, CHANG-HWAN;KIM, CHANG-JIN;YANG, YOUNG;KIM, KEUN IL;LIM, JONG-SEOK;LEE, MYEONG-SOK Sookmyung Women's University Research Institute of 2011 여성과 건강 Vol.6 No.2
The ADCYAP1 gene encodes an adenylate cyclase activating polypeptide 1. ADCYAP1 has been known to be involved in various biological processes. Multiple cytosine guanine dinucleotides (CpG island) are found in the ADCYAP1 promoter region. Transcriptional silencing by promoter hypermethylation is an important regulatory mechanism in tumorigenesis in many cancers. Therefore, the methylation level of the ADCYAP1 promoter was investigated in eight cervical cancer cell lines and human tissue samples with a distinctive degree of malignant transformation. While multiple CpG sites in the ADCYAPI promoter were highly methylated in CIN III and invasive carcinoma cells as well as seven cervical cancer cell lines, they were rarely methylated in normal cells. Importantly, methylation in the ADCYAP1 promoter seems to start from CIN I,relatively early stage of multistep carcinogenesis. This fact suggest that ADCYAP1 can be used as an effective and sensitive methylation biomarker for the early diagnosis of cervical cancer. Moreover, our data imply that the level of the ADCYAP1 promoter hypermethylation is correlated with cervical cancer development. We also show that ADCYAP1 gene expression was reactivated by the treatment of a DNA methyltransferase inhibitor of 5'-aza-2'deoxycytidine and/or a histone deacetylase inhibitor of trichostain A in cervical cancer cells suggesting that hypermethylation in the ADCYAP1 promoter is responsible for the transcriptional silencing of the ADCYAP1 gene in cervical cancer cells.
Transcriptional regulation of histidine biosynthesis genes in <i>Corynebacterium glutamicum</i>
Jung, Samil,Chun, Jae-Yeon,Yim, Sei-Heun,Lee, Soo-Suk,Cheon, Choong-Il,Song, Eunsook,Lee, Myeong-Sok Canadian Science Publishing 2010 Canadian journal of microbiology Vol.56 No.2
<P> Corynebacterium glutamicum , a gram-positive bacterium, has been widely used for industrial amino acid production. Corynebacterium glutamicum his genes are located and transcribed in two unlinked loci, hisEG and hisDCB-orf1-orf2-hisHA-impA-hisFI. The latter his operon starts the transcription at the C residue localized 196 bp upstream of the hisD ATG start codon. Our computer-based sequence analysis showed that the region corresponding to the untranslated 5′ end of the transcript, named the hisD leader region, displays the typical features of the T-box transcriptional attenuation mechanism. Therefore, expression of the cat reporter gene under the control of the wild-type or mutated hisD leader regions was tested in multi-copy (pProm and pTer series) and in single-copy (pInt series) systems under conditions of sufficient or limited histidine. Our mutational studies led to the conclusion that the CAU histidine specifier and 5′-UGGA-3′ sequence in the hisD leader region are required for the hisDCB-orf1-orf2-hisHA-impA-hisFI gene regulation. The cat gene expression from the wild-type leader region was negatively regulated by histidine. However, the cat gene expression from mutated leader regions was irresponsive to the level of histidine in the growth medium. Taken together, we propose that a T-box mediated attenuation mechanism is responsible for the gene expression of the hisDCB-orf1-orf2-hisHA-impA-hisFI operon in C. glutamicum. </P>
The Role of Vimentin as a Methylation Bio-marker for Early Diagnosis of Cervical Cancer
Samil Jung,Lisha Yi,김진선,정동준,Taejeong Oh,Chang-Hwan Kim,Chang-Jin Kim,Jin Shin,Sungwhan An,이명석 한국분자세포생물학회 2011 Molecules and cells Vol.31 No.5
Multiple cytosine guanine dinucleotides (CpG island) are found in the VIM promoter region. The levels of VIM pro-moter methylation and VIM gene expression were investi-gated in 7 cervical cancer cell lines and 50 human tissue samples with a distinctive degree of malignant trans-for-mation. While multiple CpG sites in the VIM promoter were highly methylated in CIN III and invasive carcinoma cells, they were rarely methylated in normal cells. Our result shows that methylation in the VIM promoter appears to start from CIN I and CIN II, relatively early stages of multi-step carcinogenesis. This epigenetic alteration in VIM promoter suggests the availability as a biomarker for the early diagnosis and prevention of cervical cancer. We also show that hypermethylation in the VIM promoter is re-sponsible for transcriptional silencing of the VIM gene in cervical cancer cells. In addition, our result shows that exogenous overexpression of the VIM gene in SiHa cer-vical cancer cells slightly activated cell proliferation and migration as shown in soft agar colony formation and migration assays.
The role of hLHX6-HMR as a methylation biomarker for early diagnosis of cervical cancer
Jung, Samil,Jeong, Dongjun,Kim, Jinsun,Yi, Lisha,Koo, Keunhoe,Lee, Jaehyouk,Lee, Soon-Duck,Park, Jin-Wha,Chang, Boogi,Kim, Chang-Hwan,Kim, Chang-Jin,Lee, Myeong-Sok Spandidos Publications 2010 ONCOLOGY REPORTS Vol.23 No.6
<P>The homo sapiens LIM homeobox domain LHX6 gene, hLHX6, is a putative transcription regulator with homeo-domain. Multiple cytosine guanine dinucleotides (CpG island) are found in the genomic sequences between exon 4a and exon 5 of the gene encoding hLHX6s (alternative short iso-form of hLHX6 gene). This specific CpG island, hLHX6-HMR, is found frequently hypermethylated in 7 cervical cancer cell lines as shown in MSP, BSP, and COBRA assays. Methylation densities were also investigated with human tissue samples with a distinctive degree of malignant transformation. Our data showed that the hLHX6-HMR was rarely or partly methylated in the normal and CIN I cells, respectively. In contrast, it was frequently hypermethylated in CIN II, CIN III, and invasive carcinoma cells. In summary, this methylation study led to two conclusions. First, hLHX6-HMR hypermethylation is exclusively associated with cervical carcinogenesis. Second, the epigenetic change in hLHX6-HMR seems to start at CIN I, relatively early stage of cervical cancer development. Therefore, hLHX6-HMR can be used as an effective and sensitive methylation biomarker for early diagnosis of cervical cancer.</P>
Jung, Samil,Ohk, Jiyeon,Jeong, Dongjun,Li, Chengping,Lee, Soonduck,Duan, Jingjing,Kim, Changjin,Lim, Jong-Seok,Yang, Young,Kim, Keun-Il,Lee, Myeong-Sok Lychnia 2014 International journal of oncology Vol.45 No.1
<P>The p34(SEI-1) oncoprotein is involved in a transcriptional regulation, cell cycle regulation, apoptosis, development and many other important cellular functions. Our present study suggests that p34(SEI-1) can promote metastasis by enhancing migration and invasion of cancer cells. Consistently, p34(SEI-1) expression was found to be increased as the tumor invasiveness progressed in human breast tissues. p34(SEI-1) may promote cancer metastasis by activating the PI3K/AKT signaling pathway. In this process, p34(SEI-1) activates two different serine/threonine kinases, AKT or ILK, depending on the expression status of HER2/neu oncogene. In HER2/neu suppressed cancer cells, p34(SEI-1) promoted metastasis mainly by activating AKT via phosphorylation of the 473 serine residue. In HER2/neu expressing cancer cells, p34(SEI-1) overexpression downregulates HER2/neu expression, leading to the activation of another crucial serine/threonine kinase ILK due to phosphorylation of the 178 threonine residue instead of AKT. These results suggest that p34(SEI-1) affects cancer metastasis by regulating two different signaling pathways depending on the HER2/neu expression level, in which AKT and ILK modulation can be stimulated by p34(SEI-1) overexpression.</P>
Samil Kho,Minsu Kim,Sunyoung Sohn,Donggeun Jung,Jinhyo Boo,Seonghoon Jeong,Sanghee Ko Park 한국진공학회(ASCT) 2005 Applied Science and Convergence Technology Vol.14 No.4
For the longevity of OLEDs, passivation of OLEDs is an important process step since organic materials used in OLEDs are very vulnerable to moisture. In this work, the passivation effect of the plasma polymerized para-xylene (PPpX) layers was studied. The PPpX layers deposited by PECVD were formed on top of the cathode with various plasma powers of 50?90 W. Passivation effect of PPpX was significantly dependent upon the deposition plasma power of the PPpX film. The lifetime of OLEDs with the 70 W deposited PPpX passivation layer was about 5 times longer than that of the control device.