Ching‐Shih Chen

The Ohio State University

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Co-Authors

Samuel K. Kulp

The Ohio State University

111

Dasheng Wang

The Ohio State University

Aaron M. Sargeant

Charles River Laboratories (United States)

Yu-Chieh Wang

Chung Shan Medical University

Steven K. Clinton

The Ohio State University

John C. Byrd

The Ohio State University

Po-Chen Chu

China Medical University

Che‐Ming Teng

National Taiwan University

Natarajan Muthusamy

The Ohio State University

Mei-Chuan Chen

Taipei Medical University Hospital

Cooperative Institutions

The Ohio State University

328

The Ohio State University Wexner Medical Center

130

The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute

103

National Taiwan University

Ohio University

Cornell University

Comprehensive Blood & Cancer Center

Weatherford College

National Cheng Kung University

National Yang Ming Chiao Tung University

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Supplementary Discussion from Suppression of Prostate Epithelial Proliferation and Intraprostatic Progrowth Signaling in Transgenic Mice by a New Energy Restriction-Mimetic Agent

Lisa D. Berman-Booty Po‐Chen Chu Jennifer M. Thomas‐Ahner Brad Bolon Dasheng Wang

PDF file - 120K, This is a more detailed discussion of the microarray data.

10.1158/1940-6207.22524566.v1

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Data from Small-Molecule Inhibitors of Phosphatidylinositol 3-Kinase/Akt Signaling Inhibit Wnt/β-Catenin Pathway Cross-Talk and Suppress Medulloblastoma Growth

Ninib Baryawno Baldur Sveinbjörnsson Staffan Eksborg Ching‐Shih Chen Per Kogner

<div>AbstractActivation of the β-catenin and receptor kinase pathways occurs often in medulloblastoma, the most common pediatric malignant brain tumor. In this study, we show that molecular cross-talk between the β-catenin and phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathways is crucial to sustain medulloblastoma pathophysiology. Constitutive activation of phosphoinositide-dependent protein kinase 1 (PDK1), Akt, and glycogen synthase kinase 3β (GSK-3β) was detected by immunohistochemistry in all primary medulloblastomas examined (n = 41). Small-molecule inhibitors targeting the PI3K/Akt signaling pathway affected β-catenin signaling by inhibition of GSK-3β activity, resulting in cytoplasmic retention of β-catenin and reduced expression of its target genes cyclin D1 and c-Myc. The PDK1 inhibitor OSU03012 induced mitochondrial-dependent apoptosis of medulloblastoma cells and enhanced the cytotoxic effects of chemotherapeutic drugs in a synergistic or additive manner. In vivo, OSU03012 inhibited the growth of established medulloblastoma xenograft tumors in a dose-dependent manner and augmented the antitumor effects of mammalian target of rapamycin inhibitor CCI-779. These findings demonstrate the importance of cross-talk between the PI3K/Akt and β-catenin pathways in medulloblastoma and rationalize the PI3K/Akt signaling pathway as a therapeutic target in treatment of this disease. Cancer Res; 70(1); 266–76</div>

10.1158/0008-5472.c.6500373

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Bladder cancer: Basic research (I)

The Journal of Urology (2003)

Dix P. Poppas Michael M. Maher Cathy Kelly Maria I. New New York

result.Of those patients with normal DMSA, VCUG and UIS, none developed a second febrile UTI.Of those patients with an abnormal DMSA, normal VCUG and UlS, only one developed a second febrile UTI.In children less than two years old, with normal studies (VCUG and U/S), it appears DMSA has little predictive value in the occurrence of a second febrile UTI.

10.1016/s0022-5347(03)80037-x

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Citations (1)

Bifunctional chiral synthons via biochemical methods.

Tetrahedron Letters (1985)

Shih‐Hsiung Wu Liqing Zhang Ching‐Shih Chen Gary Girdaukas Charles J. Sih

Synthon

10.1016/s0040-4039(00)98724-0

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Supplementary Figure Legends 1-8, Tables 1-3 from Small-Molecule Inhibitors of Phosphatidylinositol 3-Kinase/Akt Signaling Inhibit Wnt/β-Catenin Pathway Cross-Talk and Suppress Medulloblastoma Growth

Ninib Baryawno Baldur Sveinbjörnsson Staffan Eksborg Ching‐Shih Chen Per Kogner

10.1158/0008-5472.22382970.v1

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Retraction: Corrigendum: Insulin-like growth factor-I receptor is suppressed through transcriptional repression and mRNA destabilization by a novel energy restriction-mimetic agent

Carcinogenesis (2019)

Po-Chen Chu Samuel K. Kulp Ching‐Shih Chen

10.1093/carcin/bgz057

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Abstracts of the 2^nd Cancer Cachexia Conference, Montreal, Canada, 26–28 September 2014

Journal of Cachexia Sarcopenia and Muscle (2015)

Vickie E. Baracos Maurizio Muscaritoli Zaira Aversa Filippo Rossi Fanelli Rashami Awasthi

Cancer cachexia contributes to poor prognosis through progressive depletion of the body's energy and protein reserves; research is revealing the impact of the quantitly of these reserves on survival.Our group has exploitated computed tomography (CT) images to study body composition in cancer patients.We argue that CT taken for the purposes of diagnosis and routine follow-up can be used to derive clinically useful information on skeletal muscle and fat amount and distribution.Population-based data sets have been analyzed, revealing wide variation in individual proportions of fat and muscle (Prado et al.

10.1002/jcsm.12004

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Targeting Histone Deacetylase in Cancer Therapy

ChemInform (2006)

Hsiang‐Yu Lin Chang‐Shi Chen Hsiang‐Yu Lin Jing‐Ru Weng Ching‐Shih Chen

Abstract ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 200 leading journals. To access a ChemInform Abstract, please click on HTML or PDF.

Cancer Therapy

10.1002/chin.200638252

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Peroxisome Proliferator‐activated Receptor gamma‐Independent Repression of Prostate Specific Antigen by Troglitazone and its Derivatives in Prostate Cancer Cells

The FASEB Journal (2006)

Chih-Cheng Yang Chia‐Yu Ku Chung‐Wai Shiau Samuel K. Kulp Ching‐Shih Chen

In light of the potential use of the thiazolidinedione family of peroxisome proliferator-activated receptor-γ (PPARγ) agonists in prostate cancer treatment, this study assessed the mechanism by which these agents suppress prostate specific antigen (PSA) secretion in prostate cancer cells is independent of PPARγ activation. First, this thiazolidinedione-mediated PSA down-regulation is structure- specific irrespective of the relative PPARγ agonist potency. Second, the PPARγ-inactive analogues of troglitazone and ciglitazone (Δ2TG and Δ2CG, respectively) exhibit higher potency than the parent compound in inhibiting dihydrotestosterone (DHT)-stimulated PSA secretion. While 10 μM troglitazone and Δ2TG significantly inhibit PSA secretion, they do not alter the expression level of androgen receptor (AR) or interfere with DHT-activated nuclear translocation of AR. However, reporter gene and chromatin immunoprecipitation studies indicate that TG and Δ2TG block AR recruitment to the androgen response elements (AREs) within the PSA promoter. Thus, this study raises a question of whether the ability of oral troglitazone to reduce PSA levels in prostate cancer patients is therapeutically relevant. Furthermore, it is noteworthy that troglitazone and Δ2TG at high doses were able to inhibit AR expression. From a translational perspective, separation of PPARγ agonist activity from AR down-regulation provides a molecular basis to use troglitazone as a platform to design AR-ablative agents.

Troglitazone

Ciglitazone

Thiazolidinedione

Dihydrotestosterone

10.1096/fasebj.20.4.a464-a

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Eradication of Intracellular Salmonella enterica Serovar Typhimurium with a Small-Molecule, Host Cell-Directed Agent

Antimicrobial Agents and Chemotherapy (2009)

Hao‐Chieh Chiu Samuel K. Kulp Shilpa Soni Dasheng Wang John S. Gunn

Eradication of intracellular pathogenic bacteria with host-directed chemical agents has been an anticipated innovation in the treatment of antibiotic-resistant bacteria. We previously synthesized and characterized a novel small-molecule agent, AR-12, that induces autophagy and inhibits the Akt kinase in cancer cells. As both autophagy and the Akt kinase have been shown recently to play roles in the intracellular survival of several intracellular bacteria, including Salmonella enterica serovar Typhimurium, we investigated the effect of AR-12 on the intracellular survival of Salmonella serovar Typhimurium in macrophages. Our results show that AR-12 induces autophagy in macrophages, as indicated by increased autophagosome formation, and potently inhibits the survival of serovar Typhimurium in macrophages in association with increased colocalization of intracellular bacteria with autophagosomes. Intracellular bacterial growth was partially rescued in the presence of AR-12 by the short hairpin RNA-mediated knockdown of Beclin-1 or Atg7 in macrophages. Moreover, AR-12 inhibits Akt kinase activity in infected macrophages, which we show to be important for its antibacterial effect as the enforced expression of constitutively activated Akt1 in these cells reverses the AR-12-induced inhibition of intracellular serovar Typhimurium survival. Finally, oral administration of AR-12 at 2.5 mg/kg/day to serovar Typhimurium-infected mice reduced hepatic and splenic bacterial burdens and significantly prolonged survival. These findings show that AR-12 represents a proof of principle that the survival of intracellular bacteria can be suppressed by small-molecule agents that target both innate immunity and host cell factors modulated by bacteria.

Salmonella enterica

Intracellular parasite

10.1128/aac.00555-09

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Citations (75)