Publications (5)10.08 Total impact
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Article: SUMOylated IRF-1 shows oncogenic potential by mimicking IRF-2.
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ABSTRACT: Interferon regulatory factor-1 (IRF-1) is an interferon-induced transcriptional activator that suppresses tumors by impeding cell proliferation. Recently, we demonstrated that the level of SUMOylated IRF-1 is elevated in tumor cells, and that SUMOylation of IRF-1 attenuates its tumor-suppressive function. Here we report that SUMOylated IRF-1 mimics IRF-2, an antagonistic repressor, and shows oncogenic potential. To demonstrate the role of SUMOylated IRF-1 in tumorigenesis, we used SUMO-IRF-1 recombinant protein. Stable expression of SUMO-IRF-1 in NIH3T3 cells resulted in focus formation and anchorage-independent growth in soft agar. Inoculation of SUMO-IRF-1-transfected cells into athymic nude mice resulted in tumor formation and infiltration of adipose tissues. Finally, we demonstrated that SUMO-IRF-1 transforms NIH3T3 cells in a dose-dependent manner suggesting that SUMOylated IRF-1 may act as an oncogenic protein in tumor cells.Biochemical and Biophysical Research Communications 12/2009; 391(1):926-30. · 2.48 Impact Factor -
Article: Reduced expression of DRAM2/TMEM77 in tumor cells interferes with cell death.
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ABSTRACT: Although the role of autophagy in tumorigenesis remains controversial, recent reports support the notion that inhibition of autophagy promotes tumor formation. Damage-regulated autophagy regulator (DRAM) has been identified as an effector molecule that is critical for p53-mediated apoptosis, and we investigated whether there might be other DRAM-like molecules linking autophagy and apoptosis. In this study, we cloned a novel DRAM-homologous protein, DRAM2, and showed that the expression of DRAM2 is down-regulated in ovarian tumors. DRAM2 is mainly localized in the lysosome, and co-localizes with DRAM. While expression of DRAM or DRAM2 individually did not induce cell death, co-expression of DRAM2 with DRAM significantly induced cell death, while the silencing of endogenous DRAM2 attenuated cell death, suggesting that DRAM2 is involved in cell death. Thus, we propose that reduced expression of DRAM2 may contribute to enhanced cell survival in tumor cells.Biochemical and Biophysical Research Communications 11/2009; 390(4):1340-4. · 2.48 Impact Factor -
Article: Stool methylation-specific polymerase chain reaction assay for the detection of colorectal neoplasia in Korean patients.
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ABSTRACT: To investigate the feasibility of detecting hypermethylation in stool samples as a noninvasive screening tool for colorectal cancer and precancerous lesions, we evaluated the hypermethylation of three genes in the stool samples of patients with colorectal cancer, patients with colorectal adenomas, and healthy control subjects. Stool samples were obtained from 37 endoscopically diagnosed healthy controls, 52 patients with adenomas, and 60 patients with colorectal cancer. The methylation status of the methylguanine DNA methyltransferase, human Mut L homolog-1, and vimentin promoter in bisulfite-modified DNA was investigated in a blinded manner by methylation-specific polymerase chain reaction with primer pairs designed to amplify specifically the methylated or unmethylated alleles. The methylated methylguanine DNA methyltransferase, human Mut L homolog-1, and vimentin were detected in 51.7%, 30.0%, and 38.3% of colorectal cancer, and in 36.5%, 11.%, and 15.4% of colorectal adenomas, respectively. The sensitivities of the combined study, using three markers for the detection of colorectal cancer and colorectal adenomas, were 75.0% and 59.6%. The specificity was 86.5%. Our results have demonstrated that the promoter hypermethylation for methylguanine DNA methyltransferase, human Mut L homolog-1, and vimentin in stool samples is a feasible epigenetic marker that is a sensitive, specific, and noninvasive alternative for colorectal cancer screening. This method of screening for colorectal cancer may be useful for patients that decline screening because of fear or inconvenience.Diseases of the Colon & Rectum 09/2009; 52(8):1452-9; discussion 1459-63. · 3.13 Impact Factor -
Article: The influence of ceramic surface treatments on the tensile bond strength of composite resin to all-ceramic coping materials.
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ABSTRACT: An increasing demand for esthetic restorations has resulted in the development of new ceramic systems, but the fracture of veneering ceramics still remains the primary cause of failure. Porcelain repair frequently involves replacement with composite resin, but the bond strength between composite resin and all-ceramic coping materials has not been studied extensively. The purpose of this study was to evaluate the tensile bond strength of composite resin to 3 different all-ceramic coping materials with various surface treatments. Thirty specimens (10 x 10 x 2 mm) each of lithium-disilicate ceramic (IPS Empress2 [E]), alumina ceramic (In-Ceram Alumina [I]), and zirconia ceramic (Zi-Ceram [Z]) were fabricated. Feldspathic ceramic (Duceram Plus [F]) was used as the control. Each material was divided into 3 groups (n=10), and 3 different surface treatments were performed: airborne-particle abrasion with 50-microm alumina particles (Ab); airborne-particle abrasion with 50-microm alumina particles and acid etching with 4% hydrofluoric acid (Ae); or airborne-particle abrasion with 30-microm alumina particles modified with silica acid (Si). After surface treatment of ceramic specimens, composite resin cylinders (5-mm diameter x 10-mm height) were light polymerized onto the ceramic specimens. Each specimen was subjected to a tensile load at a crosshead speed of 2 mm/min until fracture. The fracture sites were examined with scanning electron microscopy to determine the location of failure during debonding and to examine the surface treatment effects. Two-way analysis of variance and the Duncan multiple comparison test (alpha=.05) were used to analyze the bond strength values. There were significant differences in the bond strengths for both ceramics (P<.001) and surface treatments (P<.001) and the interaction (P<.001). The Duncan analysis yielded the following statistical subsets of the bond strength values: (FAe, ISi, EAe, ZSi) > FAb > (FSi, EAb, ESi) (IAb, IAe) > (ZAe, ZAb). The results illustrate no differences within the parentheses but statistically significant differences among the groups. Alumina and zirconia ceramic specimens treated with a silica coating technique, and lithium disilicate ceramic specimens treated with airborne-particle abrasion and acid etching yielded the highest tensile bond strength values to a composite resin for the materials tested.Journal of Prosthetic Dentistry 10/2005; 94(4):357-62. · 1.32 Impact Factor -
Article: Detection of colorectal neoplasm using promoter methylation of ITGA4, SFRP2, and p16 in stool samples: a preliminary report in Korean patients.
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ABSTRACT: Colorectal cancer (CRC) screening using stool DNA has yielded a greater detection rate than conventional fecal occult blood testing. The aim of this study was to determine the sensitivity and specificity of this detection method for colorectal adenomas and carcinomas using ITGA4, SFRP2 and p16 promoter methylation. The methylation status of ITGA4, SFRP2 and p16 promoters in bisulfite-modified stool DNA was investigated in a blinded manner with methylation specific PCR (MSP) from 31 endoscopically diagnosed healthy controls, 25 patients with adenomas and 30 patients with CRC. Methylated ITGA4, SFRP2 and p16 promoters were detected in 36.7%, 60.0%, and 40.0% of the CRC samples and in 16.0%, 44.0%, and 24.0% of the colorectal adenomas, respectively. The sensitivity of the combined study using the three markers for CRC and colorectal adenoma detection was 70.0% and 72.0%. The specificity of this method was 96.8%. Our results demonstrate that ITGA4, SFRP2 and p16 promoter methylation in stool samples had high sensitivity and specificity for the detection of colorectal adenomas and CRC. This newly developed screening may be a useful non-invasive alternative screening for CRC detection.Hepato-gastroenterology 57(101):720-7. · 0.66 Impact Factor
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2005
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Yonsei University
- Department of Prosthodontics
Seoul, Seoul, South Korea
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