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MicroRNA Expression Profiles in Korean Non-Small Cell Lung Cancer
( Ji Woong Son ),( Young Jin Kim ),( Hyun Min Cho ),( Soo Young Lee ),( Jin Sung Jang ),( Jin Eun Choi ),( Jung Uee Lee ),( Min Gyu Kang ),( Yu Mi Lee ),( Sun Jung Kwon ),( Eu Gene Choi ),( Moon Jun N 대한결핵 및 호흡기학회 2009 Tuberculosis and Respiratory Diseases Vol.67 No.5
Background: MicroRNAs (miRNAs) play an important role in the regulation of cell proliferation, apoptosis, development and differentiation. Several studies have shown that aberrant expression of miRNAs is involved in cancer development and progression by regulating the expression of proto-oncogenes or tumor suppressor genes. In this study, we investigated miRNA expression profiles in Korean patients with non-small cell lung cancer (NSCLC). Methods: We performed miRNA microarray analysis containing 60∼65 bp oligonucleotide probes representing human 318 miRNAs and validated the results of the microarray with Northern blot analysis or quantitative RT-PCR. Next, we examined the correlation between miRNA expression and the target gene transcriptional profile using a human whole-genome-expression microarray. Results: We showed that 35 miRNAs were expressed differentially in the NSCLCs and corresponding non-malignant lung tissues. We showed that 35 miRNAs were expressed differentially in the NSCLCs and corresponding nonmalignant lung tissues. Thirteen of the 35 differentially expressed miRNAs were newly identified in the present study. Of the 35 miRNAs, 2 (miR-371 and miR-210) were over-expressed in lung cancers, and 33 miRNAs, including miR-145, were under-expressed in lung cancers. miR-99b expression consistently showed a negative correlation with FGFR3 expression. Conclusion: Albeit a small number of patients were examined, these results suggest that miRNA expression profiles in Korean lung cancers may be somewhat different from the expression profiles reported on lung cancers in Western populations. The findings suggest that miR-99b might be a tumor suppressor through its up-regulation of FGFR3.
Review : Year-in-Review of Lung Cancer
( Ji Woong Son ) 대한결핵 및 호흡기학회 2012 Tuberculosis and Respiratory Diseases Vol.73 No.3
In the last several years, we have made slow but steady progress in understanding molecular biology of lung cancer. This review is focused on advances in understanding the biology of lung cancer that have led to proof of concept studies on new therapeutic approaches. The three selected topics include genetics, epigenetics and non-coding RNA. This new information represents progress in the integration of molecular mechanisms that to identify more effective ways to target lung cancer.
Ji Woong Roh,Sanghoon Shin,Young-Guk Ko,Nak-Hoon Son,Chul-Min Ahn,Pil-Ki Min,Jae-Hwan Lee,Chang-Hwan Yoon,Cheol Woong Yu,Seung Whan Lee,Sang-Rok Lee,Seung Hyuk Choi,In-Ho Chae,Donghoon Choi 대한심장학회 2022 Korean Circulation Journal Vol.52 No.7
Background and Objectives: Limited data are available regarding long-term clinical outcomes of iliac artery endovascular therapy (EVT) in real-world practice. This study investigated long-term outcomes according to Trans-Atlantic Inter-Society Consensus (TASC) classifications. Methods: We analyzed data from 1,705 limbs of 1,364 patients from the retrospective cohort of the multicenter Korean Vascular Intervention Society Endovascular Therapy in Lower Limb Artery Disease registry. The primary endpoint was target lesion revascularization (TLR)-free survival. Results: TASC A, B, C, and D lesions were present in 19.4%, 26.2%, 28.7%, and 25.7% of the treated limbs, respectively. The technical success rate was 96.2% and did not differ between TASC lesion types. Complications occurred in 6.8% of cases and more occurred in TASC D (11.8%). Iliac artery EVT showed a 5-year TLR-free survival of 89.2%. The TASC D group had the lowest TLR-free rate of 79.3%. TASC D (hazard ratio [HR], 1.75; 95% confidence interval [CI], 1.12–2.73; p=0.014), plain old balloon angioplasty (HR, 4.25; 95% CI, 2.03–8.88; p<0.001), current smoker (HR, 1.89; 95% CI, 1.26–2.83; p=0.002), previous bypass surgery (HR, 3.04; 95% CI, 1.28–7.19; p=0.011), combined femoropopliteal treatment (HR, 4.89; 95% CI, 3.19–7.50; p<0.001), combined below the knee treatment (HR, 2.20; 95% CI, 1.25–3.89; p=0.007), and complications (HR, 1.86; 95% CI, 1.07–3.24; p=0.028) were predictors for TLR. Conclusions: Iliac artery EVT achieved excellent technical success and 5-year TLR-free survival. TASC D showed a favorable but lower 5-year TLR-free survival rate and higher complication rate compared with other TASC groups.
Son, Ji Woong The Korean Academy of Tuberculosis and Respiratory 2012 Tuberculosis and Respiratory Diseases Vol.73 No.3
In the last several years, we have made slow but steady progress in understanding molecular biology of lung cancer. This review is focused on advances in understanding the biology of lung cancer that have led to proof of concept studies on new therapeutic approaches. The three selected topics include genetics, epigenetics and non-coding RNA. This new information represents progress in the integration of molecular mechanisms that to identify more effective ways to target lung cancer.
( Ji Woong Son ),( Soo Young Lee ),( Hyo Sung Jeon ),( Hae Woo Lee ),( Jae Chel Lee ),( Jae Yong Park ),( Moon Jun Na ),( Yoo Sang Yoon ) 대한내과학회 2014 대한내과학회 추계학술발표논문집 Vol.2014 No.1
Background: During cancer progression, some tumor cells show changes in their plasticity by morphological and phenotypical conversions, as an expression of mesenchymal markers and loss of epithelial markers, collectively referred to as epithelial-mesenchymal transition (EMT). EMT has been increasingly recognized as a critical phenomenon in lung cancer progression. The goal of this study was to identify microRNAs involved in lung cancer progression. Methods: A microarray and qRT-PCR were performed to investigate the miRNA expression profi les in mesenchymal lung cancer cells. The role of miR-146a in lung cancer progression was measured by invasion and migration assays in vitro. Bioinformatics and luciferase report assays were used to identify the target of miR-146a Results: The expression of miR-146a was reduced in mesenchymal phenotypes. The over-expression of miR-146a induced a marked reduction of mesenchymal marker and increase epithelial marker in several lung cancer cell lines. Moreover, the over-expression of miR- 146a suppressed lung cancer cells migration and invasion. The expression of miR-146a was down-regulated in advanced lung cancer tissues. Insulin receptor substrate 2 (IRS2) was a identifi ed target of miR-146a. IRSs are adaptor proteins that link signaling from upstream activators to multiple downstream effectors to modulate normal growth, metabolism, survival, and differentiation. miR-146a regulated the expression of IRS2 mRNA and protein level. Conclusions: These data demonstrate for the fi rst time that miR-146a was down-regulated in advanced lung cancer and suppressed lung cancer progression by repressing IRS2 expression. This sheds a new insight into the post-transcriptional regulation of lung cancer progression by miRNAs, a potential approach for the treatment of lung cancer.
SON, JI WOONG,KIM, YOUNG JIN,CHO, HYUN MIN,LEE, SOO YOUNG,LEE, SU MAN,KANG, JAE‐,KU,LEE, JUNG UEE,LEE, YU MI,KWON, SUN JUNG,CHOI, EUGENE,NA, MOON JUN,PARK, JAE YONG,KIM, DONG SUN Blackwell Publishing Asia 2011 RESPIROLOGY Vol.16 No.8
<P><B>ABSTRACT</B></P><P><B>Background and objective: </B> The exact role of the cystic fibrosis transmembrane conductance regulator (CFTR) in pathophysiology, and the mechanisms regulating its expression are poorly understood. The <I>CFTR</I> gene is known to be genetically or epigenetically associated with several cancers. In the present study, the methylation status of the promoter region of the <I>CFTR</I> gene and its expression in primary non‐small cell lung cancer (NSCLC) were investigated.</P><P><B>Methods: </B> The methylation status of the promoter region of the <I>CFTR</I> gene in NSCLC tissue was assessed by pyrosequencing and methylation‐specific PCR. Expression of the <I>CFTR</I> gene was analysed by real‐time PCR, and <I>CFTR</I> gene reactivation was investigated using 5‐aza‐2′‐deoxycytidine. The correlation between methylation of the <I>CFTR</I> gene and the clinical features of the patients was assessed.</P><P><B>Results: </B> Methylation of the <I>CFTR</I> gene in NSCLC was quantitatively high by pyrosequencing analysis and qualitatively frequent by methylation‐specific PCR analysis. Expression of the <I>CFTR</I> gene was significantly lower in NSCLC compared with normal lung tissue. In addition, the demethylating agent 5‐aza‐2′‐deoxycytidine increased <I>CFTR</I> gene expression. Methylation of the <I>CFTR</I> gene was significantly greater in squamous cell carcinomas than in adenocarcinomas. <I>CFTR</I> gene methylation was associated with significantly poorer survival in young patients, but not in elderly patients.</P><P><B>Conclusions: </B> These findings suggest that DNA methylation may be important for downregulation of <I>CFTR</I> gene expression in lung cancer. Promoter hypermethylation of the <I>CFTR</I> gene may be an important prognostic factor in younger patients with NSCLC.</P>
( Ji Woong Son ),( Soo Young Lee ),( Hyo Sung Jeon ),( Hae Woo Lee ),( Jae Chel Lee ),( Jae Yong Park ),( Moon Jun Na ),( Yoo Sang Yoon ) 대한결핵 및 호흡기학회 2014 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.118 No.-
Background: During cancer progression, some tumor cells show changes in their plasticity by morphological and phenotypical conversions, as an expression of mesenchymal markers and loss of epithelial markers, collectively referred to as epithelial-mesenchymal transition (EMT). EMT has been increasingly recognized as a critical phenomenon in lung cancer progression. The goal of this study was to identify microRNAs involved in lung cancer progression. Methods: A microarray and qRT-PCR were performed to investigate the miRNA expression profiles in mesenchymal lung cancer cells. The role of miR-146a in lung cancer progression was measured by invasion and migration assays in vitro. Bioinformatics and luciferase report assays were used to identify the target of miR-146a Results: The expression of miR-146a was reduced in mesenchymal phenotypes. The over-expression of miR-146a induced a marked reduction of mesenchymal marker and increase epithelial marker in several lung cancer cell lines. Moreover, the over-expression of miR-146a suppressed lung cancer cells migration and invasion. The expression of miR-146a was down-regulated in advanced lung cancer tissues. Insulin receptor substrate 2 (IRS2) was a identified target of miR-146a. IRSs are adaptor proteins that link signaling from upstream activators to multiple downstream effectors to modulate normal growth, metabolism, survival, and differentiation. miR-146a regulated the expression of IRS2 mRNA and protein level. Conclusions: These data demonstrate for the first time that miR-146a was down-regulated in advanced lung cancer and suppressed lung cancer progression by repressing IRS2 expression. This sheds a new insight into the post-transcriptional regulation of lung cancer progression by miRNAs, a potential approach for the treatment of lung cancer.
MicroRNA Expression Profiles in Korean Non-Small Cell Lung Cancer
Son, Ji Woong,Kim, Young Jin,Cho, Hyun Min,Lee, Soo Young,Jang, Jin Sung,Choi, Jin Eun,Lee, Jung Uee,Kang, Min Gyu,Lee, Yu Mi,Kwon, Sun Jung,Choi, Eugene,Na, Moon Jun,Park, Jae Yong The Korean Academy of Tuberculosis and Respiratory 2009 Tuberculosis and Respiratory Diseases Vol.67 No.5
Background: MicroRNAs (miRNAs) play an important role in the regulation of cell proliferation, apoptosis, development and differentiation. Several studies have shown that aberrant expression of miRNAs is involved in cancer development and progression by regulating the expression of proto-oncogenes or tumor suppressor genes. In this study, we investigated miRNA expression profiles in Korean patients with non-small cell lung cancer (NSCLC). Methods: We performed miRNA microarray analysis containing 60~65 bp oligonucleotide probes representing human 318 miRNAs and validated the results of the microarray with Northern blot analysis or quantitative RT-PCR. Next, we examined the correlation between miRNA expression and the target gene transcriptional profile using a human whole-genome-expression microarray. Results: We showed that 35 miRNAs were expressed differentially in the NSCLCs and corresponding non-malignant lung tissues. We showed that 35 miRNAs were expressed differentially in the NSCLCs and corresponding nonmalignant lung tissues. Thirteen of the 35 differentially expressed miRNAs were newly identified in the present study. Of the 35 miRNAs, 2 (miR-371 and miR-210) were over-expressed in lung cancers, and 33 miRNAs, including miR-145, were under-expressed in lung cancers. miR-99b expression consistently showed a negative correlation with FGFR3 expression. Conclusion: Albeit a small number of patients were examined, these results suggest that miRNA expression profiles in Korean lung cancers may be somewhat different from the expression profiles reported on lung cancers in Western populations. The findings suggest that miR-99b might be a tumor suppressor through its up-regulation of FGFR3.