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전효성,( Ji Woong Son ),( Yi Young Choi ),( Jin Eun Choi ),( Shin Yup Lee ),( Seung Soo Yoo ),( Eungbae Lee ),( Jin Jen ),( Jae Yong Park ) 대한결핵 및 호흡기학회 2012 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.114 No.0
Objective: Telomerase reactivation has been linked to cancer development and its biology. Loss of heterozygosity at chromosome 3p has been shown to correlate with telomerase activity, however, any gene in this region was not found to regulate hTERT expression. In here, we found miR-135a which is a novel regulator hTERT. Materials and Methods: Expression of miR-135a was measured with Taqman probe in 82 non-small cell lung cancers (NSCLCs). The methylation of miR-135a promoter was investigated by bisulfite methylation assay in 173 NSCLCs and lung cancer cell lines. miR-135a precursor and miR-135a inhibitor were transfected to H1299 cell to identify that it can regulate telomerase expression. Colony formation assay was used for the function of miR-135a in lung cancer tumorigenesis. Result: miR-135a was significantly downregulated in squamous cell carcinomas (p<0.001) but not in adenocarcinomas. miR-135 down-regulation was correlated with genetic and epigenetic alteration of miR1-135. miR-135a precursor down-regulate hTERT expression through direct binding to its 3`UTR. Transfection of miR-135a in lung cancer cell significantly reduce colony formation ability than scramble miRNA and miR-135a inhibitor. Conclusions: These results suggest that loss of miR-135a expression may contribute to the gain of hTERT protein expression in lung tumorigenesis. miR-135a might play an important role in squamous cell carcinogenesis.
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비소세포폐암에서 Microsatellite Instability
전효성,김정란,손지웅,박선하,박태인,김창호,김인산,정태훈,박재용 경북대학교 병원 2001 경북대학교병원의학연구소논문집 Vol.5 No.1
연구베경:MMR 유전자의 불활성화에 의해 야기되는 뮤전적 불안정성은 발암기전의 한 부류로 인정되고 있다.저자들은 비소세포폐암의 발암과정에서의 MSI의 역할을 규명하기 위해 비소세포폐암에서 MSI의 빈도 및 MSI 유무에 따른 임상상의 차이를 조사하였다. 대상 및 방법:근치적 절제술을 받은 비소세포폐암 20예를 대상으로 하였다.동결된 폐암조직과 환자의 림프구에서 DNA를 추출한 후 3P와 9p의 15개의 marker들을 대상으로 PCR을 시행하고 7% polyacrylamide gel에서 전기영동한 후 silver 염색을 시행하였다. 암조직과 림프구 DNA의 PCR product의 band를 비교하여 MSI와 LOH를 판정하였다. 결과:1)대상환자들은 남자 19예,여자 1예였으며 모두 흡연자였고 평균 흠연력은 47 갑년이었다. 폐암의 조직형은 편평상피암 15예, 선암 4예,대세포암 1예였고, 술 후 병리학적 병기는 Ⅰ기 6예,Ⅱ기 5예, ⅢA기 7예,ⅢB기 2예였다. 2)20예 가운데 8예(40%)에서 MSI가 관찰되었으며 3예는 한 개의 marker에서,5예는 2개 이상의 marker에서 MSI가 관찰되었다. 3)LOH는 10예(50%)에서 있었으며,LOH유무에 따른 병가 및 흡연력의 차이가 없었다. 4)분석한 marker의 10% 이상에서 MSI가 관찰된 MSI-L종양은 5예였으며, 대부분의 marker에서 MSI양성인 MSI-H종양은 없었다.MSS종양과 MSI-L종양은 흡연력, 병기, 폐암 조직형 및 LOH 빈도의 유의한 차이가 없었다. 결론:비소세포폐암에서 MSI는 비교적 흔히 관찰되지만 MMR 유전자의 불활성화에 의한 MMP pathway 는 비소세포폐암의 주요 발생기전은 아닐 것으로 생각된다.향 후 비소세포폐암의 발암과정에 있어서 MMP pathway의 역할을 규명하기 위해서는 보다 많은 예를 대상으로 한 연구가 필요할 것으로 생각되며, MSI 발생기전에 관한 추가적인 연구가 필요할 것으로 생각된다. Purpose: Microsatellite instability(MSI) is frequently used as an indicator of microsatellite mutator phenotype (MMP) tumors.MSI has been observed in a percentage of non-small cell lung cancer(NSCLC).However, its role in tumorigenesis of NSCLC remains unknown.The frequency and partten of MSI in NSCLC were evaluted and clinical parameters of MSI-positive tumors with those of MSS(microsatellite stable) tumors were compared. Materials and Methods: Twenty surgically resected NSCLCs were analyzed for 15 microsatellite markers located at chromosomes 3p and 9p.The peripheral blood lymphocytes of patients were used as the source of the normal DNA. Results:1) of 20 cases, 8(40%) demonstrated MSI. 2) Instability was observed more frequently in tri- and tetra-nucleotide repeats that in dinucleotide repeats. In all cases, instability appeared as a shift of individual allelic bands. 3) LOH was observed in 10(50%) of 20 tumors analyzed. 4) Of 20 cases, MSI-H tumor(showing MSI in the majority of markers) was absent. There were 5 MSI-L tumors( showing MSI in a greater than 10% of markers). 5) No significant difference was observed between MSI-L tumors and MSI negative tumors in terms of clinicopathologic features such as pack-year history of smoking, histologic subtype, and (delete) stage of disease.There was also no significant difference in the incidence of LOH in relation to the status of MSI. Conclusion: These data strongly suggest that MSI plays different roles in lung and colon cancer.MMP pathway appears to be far less important in the tumorigenesis of NSCLC, caused mainly by cigarette smoke, with little familial tendency.(tuberculosis and Respiratory Diseases 2000,48:24-32)
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Telomerase Activity and the Risk of Lung Cancer
전효성,최진은,정득규,최의영,강효경,이원기,유승수,임정옥,박재용 대한의학회 2012 Journal of Korean medical science Vol.27 No.2
Telomerase play a key role in the maintenance of telomere length and chromosome integrity. We have evaluated the association between telomerase activity and the risk of lung cancer in peripheral blood. Telomerase activity in peripheral blood mononuclear cells was measured by a PCR-designed telomeric repeat amplification protocol in 63 lung cancer patients and 190 healthy controls that were matched for age, gender, and smoking status. Telomerase activity was significantly lower in the lung cancer patients than in controls (mean ± standard deviation; 1.32 ± 1.65 vs 2.60 ± 3.09, P < 1 × 10-4). When telomerase activity was categorized into quartiles based on telomerase activity in the controls, the risk of lung cancer increased as telomerase activity reduced (Ptrend = 1 × 10-4). Moreover, when the subjects were categorized based on the median value of telomerase activity, subjects with low telomerase activity were at a significantly increased risk of lung cancer compared to subjects with high telomerase activity (adjusted odds ratio = 3.05, 95% confidence interval = 1.60-5.82, P = 7 × 10-4). These findings suggest that telomerase activity may affect telomere maintenance, thereby contributing to susceptibility to lung cancer.
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전효성,( Yi Young Choi ),( Seung Soo Yoo ),( Shin Yup Lee ),( Jae Hee Lee ),( Seung Ick Cha ),( Chang Ho Kim ),( Eung Bae Lee ),( Jae Yong Park ) 대한결핵 및 호흡기학회 2012 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.114 No.-
Background: A number of genome-wide association (GWA) studies have reported two SNPs, rs2736100 and rs402710 at 15p15.33 containing TERT and CLPTM1L genes to contribute to lung cancer susceptibility. However, the causative functional SNP(s) for the association as well as the biologic mechanism underlying the association remains unknown. Materials and Methods: Potentially functional SNPs in the TERT/CLPTM1L locus were selected from the NIEHS website and evaluated the effects of the SNPs on lung cancer susceptibility and on survival outcomes, in a case-control study (1094 cases and 1098 controls) and in a study of 340 patients with early stage surgically resected NSCLC, respectively. The association of the SNPs with telomere length and telomerase activity was evaluated. The functional effect of SNPs was evaluated by promoter assay and EMSA. Results: Three SNPs, rs2853669 (-244 T>C), rs2736098 (A305A), and rs2736100 (IVS2 T>G) were significantly associated with the risk of lung cancer. Only the rs2853669 was significantly associated with prognosis of lung cancer. The rs2853669 had a significant association with telomere length and telomerase activity. Promoter assay and EMSA revealed that the rs2853669 lead to change promoter activity and c-Myc binding efficiency to TERT promoter. Conclusions: Our results suggest that the rs2853669 is the causative functional SNP for the association of 15p13.33 with lung cancer observed in GWA studies and that this SNP changes TERT expression and telomere length, thereby contributing to lung cancer susceptibility and prognosis.
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전효성(Hyosung Jeon),문성민(Sungmin Moon),이종원(Jongweon Lee) 한국정보과학회 2005 한국정보과학회 학술발표논문집 Vol.32 No.1
본 논문에서는 로봇이나 감시 시스템에서 주로 쓰이고 있는 배경 모델링의 정확성을 지속 시키는 방법을 제안한다. 오브젝트를 추출하려면 정확한 배경 모델이 필요하다. 정확한 배경 모델을 유지하기 위해서는 전경의 정보가 배경 모델에 반영되면 안 된다. 본 논문에서는 오브젝트의 움직임을 기반으로 한 배경 무효화 기법을 사용 하여 전경이 배경 모델에 영향을 주는 것을 방지함으로써 정확한 배경 모델을 유지하는 방법을 제안한다.
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오선희,전효성,이수영,김영진,나문준,최유진,권선중,박재용,손지웅 대한결핵 및 호흡기학회 2013 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.116 No.-
Epithelial-mensenchymal transition (EMT) is a biologic process that allows a polarized epithelial cell to enable it to assume a mesenchymal cell phenotype. EMT is a crucial mechanism for cancer progression and metastasis in non small cell lung cancer (NSCLC). Multiple complex signaling systems are required for induction of EMT because epithelial cells undergoing EMT must undergo both functional and morphologic changes. We investigated the microRNA profiles of epithelial and mesenchymal lung cancer cell line to evaluate relationship between EMT and NSCLC. miR-149a was down-regulated in mesenchymal phenotypes. Therefore, we aimed to ascertain whether or not the overexpression of miR-149a inhibits invasion of lung cancer. In this study, the expression of miR-149a was down-regulated in advanced lung cancer. Overexpression of miR-149a induced a marked reduction of mesenchymal marker and increase epithelial marker in several lung cancer cell lines. The overexpression of miR-149a inhibits the invasiveness of lung cancer. miR-149a was predicted to directly bind with the 3``-UTR site of NOTCH2 based on the TargetScan. Notch has recently been shown to promote EMT. To assess whether or not miR-149a has a functional role in the down-regulation of endogenous NOTCH2 expression, we performed qRT-PCR in lung cancer cells after transfection with negative control or miR-149a precursor. When miR-149a was over-expressed, NOTCH2 mRNA expression was diminished compared with the control group. These results suggest that miR-149a may have a function as regulators of EMT.Epithelial-mensenchymal transition (EMT) is a biologic process that allows a polarized epithelial cell to enable it to assume a mesenchymal cell phenotype. EMT is a crucial mechanism for cancer progression and metastasis in non small cell lung cancer (NSCLC). Multiple complex signaling systems are required for induction of EMT because epithelial cells undergoing EMT must undergo both functional and morphologic changes. We investigated the microRNA profiles of epithelial and mesenchymal lung cancer cell line to evaluate relationship between EMT and NSCLC. miR-149a was down-regulated in mesenchymal phenotypes. Therefore, we aimed to ascertain whether or not the overexpression of miR-149a inhibits invasion of lung cancer. In this study, the expression of miR-149a was down-regulated in advanced lung cancer. Overexpression of miR-149a induced a marked reduction of mesenchymal marker and increase epithelial marker in several lung cancer cell lines. The overexpression of miR-149a inhibits the invasiveness of lung cancer. miR-149a was predicted to directly bind with the 3``-UTR site of NOTCH2 based on the TargetScan. Notch has recently been shown to promote EMT. To assess whether or not miR-149a has a functional role in the down-regulation of endogenous NOTCH2 expression, we performed qRT-PCR in lung cancer cells after transfection with negative control or miR-149a precursor. When miR-149a was over-expressed, NOTCH2 mRNA expression was diminished compared with the control group. These results suggest that miR-149a may have a function as regulators of EMT.Epithelial-mensenchymal transition (EMT) is a biologic process that allows a polarized epithelial cell to enable it to assume a mesenchymal cell phenotype. EMT is a crucial mechanism for cancer progression and metastasis in non small cell lung cancer (NSCLC). Multiple complex signaling systems are required for induction of EMT because epithelial cells undergoing EMT must undergo both functional and morphologic changes. We investigated the microRNA profiles of epithelial and mesenchymal lung cancer cell line to evaluate relationship between EMT and NSCLC. miR-149a was down-regulated in mesenchymal phenotypes. Therefore, we aimed to ascertain whether or not the overexpression of miR-149a inhibits invasion of lung cancer. In this study, the expression of miR-149a was down-regulated in advanced lung cancer. Overexpression of miR-149a induced a marked reduction of mesenchymal marker and increase epithelial marker in several lung cancer cell lines. The overexpression of miR-149a inhibits the invasiveness of lung cancer. miR-149a was predicted to directly bind with the 3``-UTR site of NOTCH2 based on the TargetScan. Notch has recently been shown to promote EMT. To assess whether or not miR-149a has a functional role in the down-regulation of endogenous NOTCH2 expression, we performed qRT-PCR in lung cancer cells after transfection with negative control or miR-149a precursor. When miR-149a was over-expressed, NOTCH2 mRNA expression was diminished compared with the control group. These results suggest that miR-149a may have a function as regulators of EMT.
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