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Molecular mechanisms of denbinobin-induced anti-tumorigenesis effect in colon cancer cells

World Journal of Gastroenterology 2005年第20期11卷 3040-3045页

作者： Kuo-Ching Yang yih-huei uen Fat-Moon Suk Yu-Chih Liang Ying-Jan Wang Yuan-Soon Ho I-Hsuan Li Shyr-Yi Lin Department of Internal Medicine Shin Kong Wu Ho-Su Memorial Hospital Taipei Taiwan Department of Internal Medicine Taipei Medical University Taipei Taiwan China Department of Surgery Chi-Mei Foundational Medical Center Yung-Kane City Tainan Taiwan China Department of Internal Medicine Taipei Medical University Hospital Taipei Taiwan China School of Medical Technology Taipei Medical University Taipei Taiwan China Department of Environmental and Occupational Health National Cheng Kung University Medical College TainanTaiwan China Department of Internal Medicine School of Medicine Taipei Medical University Taipei Taiwan China Department of Internal Medicine School of Medicine and Department of Internal Medicine Taipei Medical University Hospital Taipei Medical University Taipei Taiwan China

AIM: To explore both the in vitro and in vivo effects of denbinobin against colon cancer cells and clarify its underlying signal pathways. METHODS: We used COLO 205 cancer cell lines and nude mice xenograft model to study the in vitro and in vivo anti-cancer effects of denbinobin. RESULTS: Denbinobin at concentration of 10-20 μmol/L dose-dependently suppressed COLO 205 cell proliferation by MTT test. Flow cytometry analysis and DNA fragmentation assay revealed that 10-20 μmol/L denbinobin treatment induced COLO 205 cells apoptosis. Western blot analysis showed that caspases 3,8,9 and Bid protein were activated by denbinobin treatment to COLO 205 cells accompanied with cytochrome c and apoptosis-inducing factor (AIF) translocation. Pretreatment of MEK 1 inhibitor (U10126), but not p38 inhibitor (SB203580) and JNK inhibitor (SP600125), reversed denbinobin-induced caspase 8, 9 and Bid activation in COLO 205 cells suggesting that extracellular signal-regulated kinase were involved in the denbinobin-induced apoptosis in COLO 205 cells. Significant regression of tumor up to 68% was further demonstrated in vivo by treating nude mice bearing COLO 205 tumor xenografts with denbinobin 50 mg/kg intraperitoneally. CONCLUSION: Our findings suggest that denbinobin could inhibit colon cancer growth both in vitro and in vivo. Activation of extrinsic and intrinsic apoptotic pathways and AIF were involved in the denbinobin-induced COLO 205 cell apoptosis.

关键词： Denbinobin Colon cancer Nude mice Apoptosis ERK pathway

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Constitutive Overexpression of Bcl-2, Survivin and ER Stress Chaperone GRP-78 Confers Intrinsic Radioresistance in Human Hepatocellular Carcinoma Cells: Insight into the Mechanistic Pathways Involved

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Journal of Cancer Therapy 2013年第2期4卷 399-407页

作者： Chih-Hsiung Wu yih-huei uen Chun-Te Ho Ya-Ting Tseng Tsan-Zon Liu Jeng-Fong Chiou Stephen Wan Leung Cancer Center and Department of Radiation Oncology Taipei Medical University and Hospital Taipei Chinese Taipei Department of General Surgery Chi-Mei Foundation Medical Center Tainan Chinese Taipei Department of Radiology and Nuclear Medicine Yuan’s General Hospital Kaohsiung Chinese Taipei Department of Surgery Taipei Medical University-Shuang Ho Hospital Taipei Chinese Taipei Graduate Institute of Medical Biotechnology Chang-Gung University Gueishan Chinese Taipei Graduate Institute of Medical Sciences Taipei Medical University Taipei Chinese Taipei

We present evidence here that abundantly expressed b-catenin-triggered NF-kB-dependent upregulation of inducible nitric oxide synthase(iNOS) found in hepatoma Mahlavu cells (RT-resistant variant designated as RR-Mal), but not in Hep 3B cells (RT-sensitive variant designated as RS-3B) is a key element contribrting to the radioresisitance through the activation of two prominent radioprotective pathways. First, high iNOS expression found in RR-Mal, but not in RS-3B cells was found to perturb calcium homeostasis that triggered ER stress response leading to the overproduction of ER chaperone GRP-78 via robust generation of cleaved ATF-6a (50 kDa) subunits and their nuclear translocation. Meanwhile, both abundantly expressed NF-κB and COX-2 found in RR-Mal cells could also provoke an increased production of PGE2 resulting in robust production of Bcl-2. Interestingly, when RR-Mal cells were treated with PDTC (a NF-κB inhibitor) or celecoxib (a COX-2 inhibitor), a concentration-dependent downregulation of Bcl-2 could be demonstrated implying that Bcl-2 overexpression was indeed mediated through NF-κB/Cox-2/PGE2 pathway. Importantly, we also unveiled that siRNA-mediated silencing of survivin in RR-Mal cells could result in a concomitant downregulation of GRP-78 due to a severe inhibition of ATF-6a (50 kDa) expression. Taken together, our data demonstrate that constitutively overexpressed b-catenin/NF-κB/iNOS and NF-κB/COX-2/PGE2 pathways that overproducing GRP-78, survivin and Bcl-2 expressions are responsible for radioresistance acquisition in RR-Mal cells. Thus, both pathways could be served as potential targets for overcoming radioresistance.

关键词： Radioresistance Hepatoma Cells Inducible Nitric Oxide Synthase Bcl-2 Survivin GRP-78

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A secure threshold Paillier proxy signature scheme

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Journal of Zhejiang University-Science C(Computers and Electronics) 2010年第3期11卷 206-213页

作者： Pei-yih TING Chia-huei HSEU Department of Computer Science and Engineering National Taiwan Ocean University

As e-commerce applications and the underlying public key infrastructure have become more popular over time,many digital mechanisms emulating traditional business activities have been developed and deployed. To build a full-fledgedsecure digital world,secure implementations of more commercial activity primitives are required. In this paper,we present asecure proxy signature scheme and its threshold version based on the homomorphic Paillier cryptosystem,which can be used inmany e-commerce applications such as e-voting,e-bidding/auction,and privacy-preserving data mining. These two schemes areexistentially unforgeable against chosen-message attacks and chosen-warrant attacks in the random oracle model. Although it isbased on factoring,the threshold Paillier proxy scheme operates without requiring any trusted dealer or combiner. Thus,these twoschemes are practical for integration in modularized secure multi-party protocols.

关键词： Paillier proxy signature Threshold scheme Secure multi-party protocols Cryptographic primitives

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Clinical characteristics of patients with congenital long QT syndrome and bigenic mutations

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Chinese Medical Journal 2014年第8期127卷 1482-1486页

作者： Juang Jyh-Ming Jimmy Chen Ching-Yu Yeh huei-Ming Chiu Wei-yih Yu Chih-Chieh Liu Yen-Bin Tsai Chia-Ti Lo Li-Wei Yeh Shih-Fan Sherri Lai Ling-Ping Cardiovascular Center and Division of Cardiology Department of Internal Medicine Department of Anesthesiology Department of Environmental and Occupational Medicine Division of Endocrinology and Metabolism Department of Internal Medicine Taiwan University Hospital and Taiwan University College of Medicine Taipei Taiwan China

Background Congenital long QT syndrome （LQTS） is an ion channelopathy associated with genetic mutations. It is well known that most LQTS patients （91%） have a single mutation. The purpose of this study was to investigate the clinical characteristics of congenital LQTS patients with bigenic mutations in Taiwan, China. Methods Congenital LQTS patients were recruited consecutively at Taiwan University Hospital in Taiwan from 2003 to 2009. The diagnosis of LQTS was defined by an LQTS Schwartz score greater than 4. Mutation screening in KCNQ1, KCNH2, KCNE1, and SCN5A was performed using direct sequencing. Results Three of 16 LQTS patients （18.7%） were identified with bigenic mutations. One patient had missense mutations in KCNQ1 and KCNH2, the second in KCNQ1 and KCNE1, and the third in KCNH2 and SCN5A. The mean age at onset of LQTS for patients with bigenic mutations was （17±3） years, and all of these patients were female. Two of them experienced seizure and one presented with syncope, although one of them had a family history of syncope. The mean QTc interval was （515＋17） ms, similar to those with single mutation or SNPs （（536~74） ms, P=-0.63）. Compared to those LQTS patients with single mutation or SNPs, a significantly higher percentage of LQTS patients with bigenic mutations presented with seizure and were younger at onset of the first index event （P=0.03 and 0.001, respectively）, but lower percentage of them presented with sudden cardiac death （P=0.03）. Conclusions Although the percentage of bigenic mutations in LQTS is less than 10% in Caucasian populations, we identified 3 of 16 LQTS patients （18.7%, 95% confidence interval： 0.04-0.46） with bigenic mutations in Taiwan. However, the sevedtv of their clinical presentations was not hioher than those patients with sinele mutation or SNPs.

关键词： long QTsyndrome genetic mutation Taiwan Chinese

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