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Yeo, Marie,Kwak, Mi Sun,Kim, Dong Kyu,Chung, In Sik,Moon, Byoung Seok,Song, Keun Seog,Hahm, Ki-Baik The Society for Free Radical Research Japan 2006 Journal of clinical biochemistry and nutrition Vol.38 No.1
<P>The H<SUP>+</SUP>/K<SUP>+</SUP>-ATPase of gastric parietal cell exchanges luminal K<SUP>+</SUP> for cytoplasmic H<SUP>+</SUP>, of which outcome is gastric acidification with outflux of hydronium ion (H<SUB>3</SUB>O<SUP>+</SUP>). Secretion of gastric acid from the H<SUP>+</SUP>/K<SUP>+</SUP>-ATPase is stimulated by neuronal sensing and elaborately regulated various neuronal transmitters and hormones, consequently resulting in anchoring of the H<SUP>+</SUP>/K<SUP>+</SUP>-ATPase in canaliculi membrane of gastric parietal cell. Since hypersecretion of gastric acid or a defect of its barrier function is considered as a principal casual factor in the acid-related diseases such as duodenal and gastric ulcer, reflux esophagitis, and some types of gastritis, the development of anti-secretory agents including PPIs (proton pump inhibitors) and H2-RAs (histamine type 2 receptor antagonists) has revolutionized during the second millennium. Similar considerations applying to design of compounds substituting K<SUP>+</SUP> led to the development of acid pump antagonists (APAs), of which advantages are independent of secretory status, no lag time required, reversible in actions allowing “on-demand dosage”. Our recent studies revealed that these inhibitors of H<SUP>+</SUP>/K<SUP>+</SUP>-ATPase could be extensively applied for the selective induction of cancer cell apoptosis, a significant anti-inflammatory and gastroprotective action far beyond acid suppression. In the current review, we described the mechanistic regulation of gastric acid secretion with pump inhibitor, the difference and characteristics between PPI and APA based on the molecular mechanism, and their new applications beyond acid suppression.</P>
Yeo, Marie,Rha, Sung Young,Jeung, Hei Cheul,Hu, Shen Xiong,Yang, Sang Hwa,Kim, Yang Seok,An, Sung Whan,Chung, Hyun Cheol Wiley Subscription Services, Inc., A Wiley Company 2005 International journal of cancer: Journal internati Vol.114 No.3
<P>Ribozyme possesses specific endoribonuclease activity and catalyzes the hydrolysis of specific phosphodiester bonds, which results in the cleavage of target RNA sequences. Here, we evaluated the ability of hammerhead ribozymes targeting human telomerase RNA (hTR) to inhibit the catalytic activity of telomerase and the proliferation of cancer cells. Hammerhead ribozymes were designed against 7 NUX sequences located in open loops of the hTR secondary structure. We verified the ribozyme specificity by in vitro cleavage assay by using a synthetic RNA substrate. Subsequently, we introduced ribozyme expression vector into human breast tumor MCF-7 cells and assessed the biologic effects of ribozyme. Hammerhead ribozyme R1 targeting the template region of hTR efficiently cleaved hTR in vitro, and stable transfectants of this ribozyme induced the degradation of target hTR RNA and attenuated telomerase activity in MCF-7 cells. Moreover, the ribozyme R1 transfectant displayed a significant telomere shortening and a lower proliferation rate than parental cells. Clones with reduced proliferation capacity showed enlarged senescence-like shapes or highly differentiated dendritic morphologies of apoptosis. In conclusion, the inhibition of telomerase activity by hammerhead ribozyme targeting the template region of the hTR presents a promising strategy for inhibiting the growth of human breast cancer cells. © 2004 Wiley-Liss, Inc.</P>
Prognostic significance of Heat Shock Protein 90 in Hepatocellular Carcinoma (초)
( Marie Yeo ),( Hee Jin Park ),( Young Mi Na ),( Dong Kyu Kim ),( Jung A Lee ),( Jae Youn Cheong ),( Kwang Jae Lee ),( Hee Jeong Wang ),( Sung Won Cho ) 대한간학회 2010 Clinical and Molecular Hepatology(대한간학회지) Vol.16 No.3(S)
The loss of phenol sulfotransferase 1 in hepatocellular carcinogenesis
Yeo, Marie,Mi Na, Young,Kyu Kim, Dong,Bae Kim, Young,Jeong Wang, Hee,Lee, Jung A.,Youn Cheong, Jae,Jae Lee, Kwang,Paik, Young-Ki,Won Cho, Sung WILEY-VCH Verlag 2010 Proteomics Vol.10 No.2
<P>Biomarkers for the detection of early hepatocellular carcinoma (HCC) are urgently needed. To identify biomarkers of HCC, we performed a comparative proteomics analysis, based on 2-DE of HCC tissues and surrounding non-tumor tissues. Six xenobiotic enzymes were significantly down-regulated in the HCC tissue. Among these, phenol sulfotransferase (SULT1A1) was confirmed by Western blot analysis in 105 HCC patients. SULT1A1 showed a significant decrease in 98.1% of the HCC tissues, with 88.6% sensitivity and 66.7% specificity for the detection of HCC. Immunohistochemistry for SULT1A1 was performed and compared with glypican-3, which is a well-known marker of HCC. The results showed down-regulation of SULT1A1 and up-regulation of glypican-3 in 52.6 and 71.9% of the HCCs, and the use of both markers improved the sensitivity up to 78.9%. Moreover, SULT1A1 was useful in differentiating early HCC from benign dysplastic nodules. Clinically, the down-regulation of SULT1A1 was closely associated with an advanced International Union Against Cancer stage and high levels of serum α-fetoprotein. In conclusion, the results of this study demonstrate that the loss of SULT1A1 appears to be a characteristic molecular signature of HCC. SULT1A1 might be a useful biomarker for the detection of early HCC and help predict the clinical outcome of patients with HCC.</P>
Loss of transgelin in repeated bouts of ulcerative colitis-induced colon carcinogenesis
Yeo, Marie,Kim, Dong-Kyu,Park, Hee Jin,Oh, Tae Young,Kim, Jang Hee,Cho, Sung Won,Paik, Young-Ki,Hahm, Ki-Baik WILEY-VCH 2006 Proteomics Vol. No.
<P>Though ulcerative colitis (UC)-associated colon cancer develops from dysplastic lesions caused by chronic inflammation, the specific mechanistic link between chronic inflammation and carcinogenesis in colon has not been integrated into molecular understanding. We therefore established an experimental animal model for colitic cancer, and used proteomic analysis, based on 2-DE and MALDI-TOF MS, to identify proteins involved in colitic cancer. In our model, 6-week-old C57BL/6J mice were exposed to 15 cycles of dextran sodium sulfate (DSS), with each cycle consisting of 0.7% DSS for 1 week followed by distilled water for 10 days. Colorectal tumors developed in 22 of 24 mice (91.6%), with a tumor multiplicity of 1.727 per tumor-bearing mouse. Comparative 2-DE analysis showed that 38 protein spots were differentially expressed in colon tumors and normal colon. We identified 27 of these proteins, including GRP94, HSC70, enolase, prohibitin, and transgelin. The reduction of transgelin expression in mouse colon tumors was confirmed by Western blotting and immunohistochemistry. We also found that transgelin expression was significantly reduced in human colon tumors compared with adjacent nontumorous tissues. In conclusion, these results suggest that loss of transgelin could be a candidate for biomarker of repeated colitis-associated colon cancer.</P>
Yeo, Marie,Park, Hee Jin,Kim, Dong-Kyu,Kim, Young Bae,Cheong, Jae Youn,Lee, Kwang Jae,Cho, Sung Won Wiley Subscription Services, Inc., A Wiley Company 2010 Cancer Vol.116 No.11
<B>BACKGROUND:</B><P>We previously found the down-expression of SM22 in an experimental animal model of colorectal cancer by performing a proteomic analysis. In this study, we addressed the expression and molecular mechanisms of SM22 in human colorectal cancer.</P><B>METHODS:</B><P>To evaluate the expression of SM22 in colon cancers, Western blot and immunohistochemistry were performed in 13 normal, 14 adenomas, and 44 adenocarcinomas. To address the role of SM22 in colon carcinogenesis, SM22 was restored in the colon cancer cells by the transfection with the pIRES2 vector containing full-length SM22 cDNA and tested for tumorigenicity in vivo and in vitro.</P><B>RESULTS:</B><P>SM22 was found to be significantly down-regulated in adenocarcinoma (58%) compared with adenoma (21.4%) and normal (15.3%). The loss of SM22 correlated with poor differentiation of tumor (P = 0.009) and lymph node metastasis (P = 0.029). Restoration of SM22 expression inhibited cell migration, colony-forming ability of cancer cells, and induced retardation of in vivo tumor growth in a xenograft model.</P><B>CONCLUSIONS:</B><P>Loss of SM22 is a molecular signature of colon cancer and is closely associated with progression, differentiation, and metastasis of colon cancer. The restoration of SM22 leads to an inhibition of colon carcinogenesis in vivo and in vitro, suggesting that SM22 might potentially function as a novel tumor suppressor. Cancer 2010. © 2010 American Cancer Society.</P>