Research Topics
Genomes and Genes
| Yi SunSummaryAffiliation: Pfizer Global Research and Development Country: USA Publications
| Collaborators
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Detail Information
Publications
SAG/ROC/Rbx/Hrt, a zinc RING finger gene family: molecular cloning, biochemical properties, and biological functionsY Sun
Cancer Molecular Sciences, Pfizer Global Research and Development, Ann Arbor Laboratories, MI 48105, USA
Antioxid Redox Signal 3:635-50. 2001..Blocking SAG expression via antisense transfection inhibits tumor cell growth. Thus, SAG appears to be a valid drug target for anticancer therapy...- Seeing is believing: visualization of transcriptional activity of p53Yi Sun
Cancer Molecular Sciences, Pfizer Global Research and Development, Ann Arbor Laboratories, 2800 Plymouth Road, Ann Arbor, Michigan 48105, USA
Cancer Biol Ther 2:203-5. 2003 
Radiosensitization of human pancreatic cancer cells by MLN4924, an investigational NEDD8-activating enzyme inhibitorDongping Wei
Division of Radiation and Cancer Biology, Department of Radiation Oncology, University of Michigan, Ann Arbor, Michigan 48109, USA
Cancer Res 72:282-93. 2012..Our findings offer proof-of-concept for use of MLN4924 as a novel class of radiosensitizer for the treatment of pancreatic cancer...- Radiosensitization of head and neck squamous cell carcinoma by a SMAC-mimetic compound, SM-164, requires activation of caspasesJie Yang
Division of Radiation and Cancer Biology, Department of Radiation Oncology, University of Michigan, Ann Arbor, Michigan, USA
Mol Cancer Ther 10:658-69. 2011..Thus, SM-164 is a potent radiosensitizer via a mechanism involving caspase activation and holds promise for future clinical development as a novel class of radiosensitizer for the treatment of a subset of head and neck cancer patients... - Validation of SAG/RBX2/ROC2 E3 ubiquitin ligase as an anticancer and radiosensitizing targetLijun Jia
Department of Radiation Oncology, University of Michigan Comprehensive Cancer Center, Ann Arbor, Michigan, USA
Clin Cancer Res 16:814-24. 2010..To investigate whether SAG serves as an anticancer target, we determined the effect of SAG silencing on cell proliferation, survival, and radiosensitivity... - SAK, a new polo-like kinase, is transcriptionally repressed by p53 and induces apoptosis upon RNAi silencingJun Li
Department of Radiation Oncology, University of Michigan Comprehensive Cancer Center, 4304 CCGC, 1500 East Medical Center Drive, Ann Arbor, MI 48109 0936, USA
Neoplasia 7:312-23. 2005..Thus, SAK repression by p53 is likely mediated through the recruitment of HDAC repressors, and SAK repression contributes to p53-induced apoptosis... - Efficacy of MDM2 inhibitor MI-219 against lung cancer cells alone or in combination with MDM2 knockdown, a XIAP inhibitor or etoposideMin Zheng
Division of Radiation and Cancer Biology, Department of Radiation Oncology, University of Michigan Comprehensive Cancer Center, 4424B MS I, 1301 Catherine Street, Ann Arbor, MI 48109 5637, USA
Anticancer Res 30:3321-31. 2010..In combination, MI-219-induced cytotoxicity was not affected by MDM2 knockdown nor by a XIAP inhibitor, but MI-219 sensitized cancer cells to etoposide, suggesting MI-219 could serve as a chemosensitizing agent... - SAG/ROC2/Rbx2 is a novel activator protein-1 target that promotes c-Jun degradation and inhibits 12-O-tetradecanoylphorbol-13-acetate-induced neoplastic transformationQingyang Gu
Department of Radiation Oncology, University of Michigan Comprehensive Cancer Center, 1500 East Medical Center Drive, Ann Arbor, MI 48109, USA
Cancer Res 67:3616-25. 2007..41 preneoplastic model. Thus, AP-1/SAG establishes an autofeedback loop, in which on induction by AP-1, SAG promotes c-Jun ubiquitination and degradation, thus inhibiting tumor-promoting activity of AP-1... - A small molecule that disrupts Mdm2-p53 binding activates p53, induces apoptosis and sensitizes lung cancer cells to chemotherapySteven H Sun
Division of Cancer Biology, Department of Radiation Oncology, University of Michigan Comprehensive Cancer Center, Ann Arbor, Michigan 48109, USA
Cancer Biol Ther 7:845-52. 2008..Thus, MI-43 or its analogues could be further developed as a novel class of anticancer drug for lung cancer cells harboring wt p53 as a single agent or in combination with chemo-drugs... 
Smac-mimetic compound SM-164 induces radiosensitization in breast cancer cells through activation of caspases and induction of apoptosisDong Yang
Division of Radiation and Cancer Biology, Department of Radiation Oncology, University of Michigan, 4424B Medical Science I, 1301 Catherine Street, Ann Arbor, MI 48109 5637, USA
Breast Cancer Res Treat 133:189-99. 2012..Our study demonstrates that IAPs are valid radiosensitizing targets in breast cancer cells and SM-164 could be further developed as a novel class of radiosensitizers for the treatment of radioresistant breast cancer...- SAG/ROC2 E3 ligase regulates skin carcinogenesis by stage-dependent targeting of c-Jun/AP1 and IkappaB-alpha/NF-kappaBQingyang Gu
Department of Radiation Oncology, University of Michigan Comprehensive Cancer Center, Ann Arbor, MI 48109, USA
J Cell Biol 178:1009-23. 2007.... - SAG/ROC-SCF beta-TrCP E3 ubiquitin ligase promotes pro-caspase-3 degradation as a mechanism of apoptosis protectionMingjia Tan
Department of Radiation Oncology, University of Michigan Comprehensive Cancer Center, 1500 East Medical Center Drive, Ann Arbor, MI 48109 0936, USA
Neoplasia 8:1042-54. 2006..Thus, pro-caspase-3 appears to be a substrate of SAG/ROC-SCF(beta-TrCP) E3 Ub ligase, which protects cells from apoptosis through increased apoptosis threshold by reducing the basal level of pro-caspase-3... - Growth inhibition and radiosensitization of glioblastoma and lung cancer cells by small interfering RNA silencing of tumor necrosis factor receptor-associated factor 2Min Zheng
Division of Radiation and Cancer Biology, Department of Radiation Oncology, University of Michigan, Ann Arbor, MI 48109 5637, USA
Cancer Res 68:7570-8. 2008..Our studies suggest that TRAF2 is an attractive drug target for anticancer therapy and radiosensitization... - SAG/RBX2/ROC2 E3 ubiquitin ligase is essential for vascular and neural development by targeting NF1 for degradationMingjia Tan
Division of Radiation and Cancer Biology, Department of Radiation Oncology, University of Michigan, Ann Arbor, MI 48109, USA
Dev Cell 21:1062-76. 2011..Collectively, our study identifies NF1 as a physiological substrate of SAG-CUL1-FBXW7 E3 ligase and establishes a ubiquitin-dependent regulatory mechanism for the NF1-RAS pathway during embryogenesis... - SM-164: a novel, bivalent Smac mimetic that induces apoptosis and tumor regression by concurrent removal of the blockade of cIAP-1/2 and XIAPJianfeng Lu
University of Michigan Comprehensive Cancer Center, Ann Arbor, MI, USA
Cancer Res 68:9384-93. 2008..Furthermore, our data provide evidence that SM-164 is a promising new anticancer drug for further evaluation and development... - Induction of p21-dependent senescence by an NAE inhibitor, MLN4924, as a mechanism of growth suppressionLijun Jia
Division of Radiation and Cancer Biology, Department of Radiation Oncology, University of Michigan, 4424B Medical Science I, Ann Arbor, MI 48109, USA
Neoplasia 13:561-9. 2011..Our study reveals a novel mechanism of MLN4924 action and showed that MLN4924 could be further developed as an effective anticancer agent by inducing apoptosis and irreversible senescence... - ROC1/RBX1 E3 ubiquitin ligase silencing suppresses tumor cell growth via sequential induction of G2-M arrest, apoptosis, and senescenceLijun Jia
Division of Radiation and Cancer Biology, Department of Radiation Oncology, University of Michigan Comprehensive Cancer Center, Ann Arbor, Michigan, USA
Cancer Res 69:4974-82. 2009..Thus, ROC1 silencing triggers multiple death and growth arrest pathways to effectively suppress tumor cell growth, suggesting that ROC1 may serve as a potential anticancer target... - CK2 phosphorylation of SAG at Thr10 regulates SAG stability, but not its E3 ligase activityHongbin He
Division of Cancer Biology, Department of Radiation Oncology, University of Michigan Comprehensive Cancer Center, 4304 CCGC, 1500 East Medical Center Drive, Ann Arbor, MI 48109 0936, USA
Mol Cell Biochem 295:179-88. 2007..These studies suggested that CK2 might regulate SAG-SCF E3 ligase activity through modulating SAG's stability, rather than its enzymatic activity directly... - Disruption of Sag/Rbx2/Roc2 induces radiosensitization by increasing ROS levels and blocking NF-kappaB activation in mouse embryonic stem cellsMingjia Tan
Division of Radiation and Cancer Biology, Department of Radiation Oncology, University of Michigan, Ann Arbor, MI 48109, USA
Free Radic Biol Med 49:976-83. 2010.... - SAG/ROC2/RBX2 E3 ligase promotes UVB-induced skin hyperplasia, but not skin tumors, by simultaneously targeting c-Jun/AP-1 and p27Hongbin He
Department of Radiation Oncology, University of Michigan Comprehensive Cancer Center, 1500 East Medical Center Drive, Ann Arbor, MI 48109, USA
Carcinogenesis 29:858-65. 2008..Thus, by simultaneously targeting c-Jun and p27, SAG accelerates UVB-induced skin hyperplasia, but not carcinogenesis... - p27 degradation by an ellipticinium series of compound via ubiquitin-proteasome pathwayDeepika Pamarthy
Division of Cancer Biology, Department of Radiation Oncology, University of Michigan Comprehensive Cancer Center, Ann Arbor, Michigan 48109 0936, USA
Cancer Biol Ther 6:360-6. 2007..The finding could provide a new tool to further understand the mechanism of p27 degradation... - Cardiac glycosides inhibit p53 synthesis by a mechanism relieved by Src or MAPK inhibitionZhen Wang
Department of Radiation Oncology, University of Michigan Comprehensive Cancer Center, Ann Arbor, 48109, USA
Cancer Res 69:6556-64. 2009..The drugs may be useful in the treatment of human cancers with a gain-of-function p53 mutation... - RBX1 (RING box protein 1) E3 ubiquitin ligase is required for genomic integrity by modulating DNA replication licensing proteinsLijun Jia
Division of Radiation and Cancer Biology, Department of Radiation Oncology, University of Michigan, Ann Arbor, Michigan 48109, USA
J Biol Chem 286:3379-86. 2011..RBX-1 silencing also induces lethality during development of embryos and in adulthood. Thus, RBX1 E3 ligase is essential for the maintenance of mammalian genome integrity and the proper development and viability in C. elegans... - CUL4B ubiquitin ligase in mouse development: a model for human X-linked mental retardation syndrome?Yongchao Zhao
Division of Radiation and Cancer Biology, Department of Radiation Oncology, University of Michigan, 4424B MS 1, 1301 Catherine Street, Ann Arbor, MI 48109, USA
Cell Res 22:1224-6. 2012..Viable Cul4b-null mice provide the first animal model to study neuronal and behavioral deficiencies seen in human CUL4B XLMR patients... - DEPTOR, an mTOR inhibitor, is a physiological substrate of SCF(βTrCP) E3 ubiquitin ligase and regulates survival and autophagyYongchao Zhao
Division of Radiation and Cancer Biology, Department of Radiation Oncology, University of Michigan, Ann Arbor, MI 48109, USA
Mol Cell 44:304-16. 2011..Furthermore, DEPTOR accumulates upon glucose deprivation and mTOR inhibition to induce autophagy. Thus, βTrCP-DEPTOR-mTOR intertwine to regulate cell survival and autophagy... - Mdm2 ligase dead mutants did not act in a dominant negative manner to re-activate p53, but promoted tumor cell growthManju Swaroop
Cancer Molecular Sciences, Pfizer Global Research and Development, Ann Arbor Laboratories, 2800 Plymouth Road, Ann Arbor, MI 48105, USA
Anticancer Res 23:3167-74. 2003..Thus, ligase dead mutants of Mdm2 did not act in a dominant negative manner to reactivate p53 and they are not oncogenes in MCF10A cells... - Temporal activation of p53 by a specific MDM2 inhibitor is selectively toxic to tumors and leads to complete tumor growth inhibitionSanjeev Shangary
Comprehensive Cancer Center and Department of Internal Medicine, University of Michigan, 1500 East Medical Center Drive, Ann Arbor, MI 48109, USA
Proc Natl Acad Sci U S A 105:3933-8. 2008..MI-219 activates p53 in normal tissues with minimal p53 accumulation and is not toxic to animals. MI-219 warrants clinical investigation as a new agent for cancer treatment... - RBX1/ROC1 disruption results in early embryonic lethality due to proliferation failure, partially rescued by simultaneous loss of p27Mingjia Tan
Division of Radiation and Cancer Biology, Department of Radiation Oncology, University of Michigan Comprehensive Cancer Center, 4424B MS I, 1301 Catherine Street, Ann Arbor, MI 48109 5936, USA
Proc Natl Acad Sci U S A 106:6203-8. 2009..Our study demonstrates that the in vivo physiological function of RBX1 is to ensure cell proliferation by preventing p27 accumulation during the early stage of embryonic development... - Identification and characterization of two splicing variants of human NoxaZhen Wang
Division of Cancer Biology, Department of Radiation Oncology, University of Michigan Comprehensive Cancer Center, Ann Arbor, MI, USA
Anticancer Res 28:1667-74. 2008..Unlike Noxa, BH3-less variants failed to potentiate apoptosis induced by etoposide. Thus, Noxa variants are unlikely to play a role in apoptosis regulation... - E3 ubiquitin ligases as cancer targets and biomarkersYi Sun
Division of Cancer Biology, Department of Radiation Oncology, University of Michigan Comprehensive Cancer Center, Ann Arbor, MI 48109 0936, USA
Neoplasia 8:645-54. 2006..This would eventually lead to the development of a novel class of anticancer drugs targeting specific E3 ubiquitin ligases, as well as the development of sensitive biomarkers for cancer treatment, diagnosis, and prognosis... - AMPK-beta1 subunit is a p53-independent stress responsive protein that inhibits tumor cell growth upon forced expressionJun Li
Cancer Molecular Sciences, Pfizer Global Research and Development, Ann Arbor Laboratories, 2800 Plymouth Road, MI 48105, USA
Carcinogenesis 24:827-34. 2003..In both lines, forced AMPK-beta1 expression inhibits tumor cell growth, suggesting that AMPK-beta1 induction may facilitate stress-induced growth inhibition and cell killing... - A small molecule Smac-mimic compound induces apoptosis and sensitizes TRAIL- and etoposide-induced apoptosis in breast cancer cellsKatrina M Bockbrader
Department of Radiation Oncology, Division of Cancer Biology, University of Michigan Comprehensive Cancer Center, 4304 CCGC, 1500 East Medical Center Drive, Ann Arbor, MI 48109-0936, USA
Oncogene 24:7381-8. 2005..Thus, in these cell lines, Smac-mimic acts in an apparent IAPs dependent manner to induce apoptosis alone as well as sensitizes breast cancer cells to TRAIL or etoposide induced apoptosis via caspase-3 activation... - Early NFkappaB activation is inhibited during focal cerebral ischemia in interleukin-1beta-converting enzyme deficient miceFeng-Peng Huang
Department of Surgery (Neurosurgery, University of Michigan, Ann Arbor, USA
J Neurosci Res 73:698-707. 2003..Because cerebral ischemia induced infarction is significantly reduced in ICE KO mice, we conclude that early NFkappaB phosphorylation plays a disruptive role in the ischemic process... - Targeting the mTOR-DEPTOR pathway by CRL E3 ubiquitin ligases: therapeutic applicationYongchao Zhao
Division of Radiation and Cancer Biology, Department of Radiation Oncology, University of Michigan, Ann Arbor, MI 48109, USA
Neoplasia 14:360-7. 2012.... - Targeting E3 ubiquitin ligases for cancer therapyYi Sun
Division of Cancer Biology, Department of Radiation Oncology, University of Michigan Comprehensive Cancer Center, Ann Arbor, Michigan 48109 0936, USA
Cancer Biol Ther 2:623-9. 2003..Emerging technologies, such as siRNA, will provide a better validation of many E3s. It is anticipated that E3 ubiquitin ligases will represent an important new target platform for future mechanism-driven drug discovery... - Overview of approaches for screening for ubiquitin ligase inhibitorsYi Sun
Division of Cancer Biology, Department of Radiation Oncology, University of Michigan, Ann Arbor, Michigan, USA
Methods Enzymol 399:654-63. 2005..Experimental details for many of these assays can be found in other chapters in this volume... - Chemosensitization by emodin, a plant-derived anti-cancer agent: mechanism of actionYi Sun
Division of Cancer Biology, Department of Radiation Oncology, The University of Michigan, 4304 Cancer Center, 1500 E. Medical Center Dr, Ann Arbor, MI 48109, USA
Cancer Biol Ther 7:476-8. 2008 - p53 and its downstream proteins as molecular targets of cancerYi Sun
Division of Cancer Biology, Department of Radiation Oncology, University of Michigan Comprehensive Cancer Center, Ann Arbor, Michigan 48109-0936, USA
Mol Carcinog 45:409-15. 2006..If a therapeutic window is obtained, a SAK inhibitor identified from high throughput screening (HTS) could serve as a lead compound for development of a novel class of apoptosis-inducing anticancer drugs... - Functional characterization of SAG/RBX2/ROC2/RNF7, an antioxidant protein and an E3 ubiquitin ligaseYi Sun
Division of Radiation and Cancer Biology, Department of Radiation Oncology, University of Michigan, 4424B Medical Science I, 1301 Catherine Street, Ann Arbor, MI 48109, USA
Protein Cell 4:103-16. 2013..Given its major role in promoting targeted degradation of tumor suppressive proteins, leading to apoptosis suppression and accelerated tumorigenesis, SAG E3 ligase appears to be an attractive anticancer target... - Histone deacetylase 5 is not a p53 target gene, but its overexpression inhibits tumor cell growth and induces apoptosisYuanhui Huang
Cancer Molecular Sciences, Pfizer Global Research and Development, Ann Arbor Laboratories, 2800 Plymouth Road, Ann Arbor, MI 48105, USA
Cancer Res 62:2913-22. 2002..Induction of TNFR1, TNFSF7, and caspase-8 were confirmed by Northern and Western analyses. Thus, activation of tumor necrosis factor death receptor pathway appears to be associated with HDAC5-induced spontaneous apoptosis... - RASSF1A, a critical gene inactivated during nasopharyngeal carcinogenesis?Yi Sun
Division of Cancer Biology, Department of Radiation Oncology, The University of Michigan Comprehensive Cancer Center, Ann Arbor, Michigan 48109, USA
Cancer Biol Ther 4:1123-4. 2005 - Insulin-like growth factor receptor-1 as an anti-cancer target: blocking transformation and inducing apoptosisYuli Wang
Cancer Molecular Sciences, Pfizer Global Research and Development, Ann Arbor Laboratories, 2800 Plymouth Road, Ann Arbor, MI 48105, USA
Curr Cancer Drug Targets 2:191-207. 2002..Cancer patients could eventually benefit from the development of these specific IGF-IR antagonists... - Autocrine human growth hormone inhibits placental transforming growth factor-beta gene transcription to prevent apoptosis and allow cell cycle progression of human mammary carcinoma cellsRalph Graichen
Institute of Molecular and Cell Biology, 30 Medical Drive, Singapore 117609, Republic of Singapore
J Biol Chem 277:26662-72. 2002..Such transcriptional repression of negative regulatory factors, such as PTGF-beta, may also be requisite for direct stimulation of mammary carcinoma cell mitogenesis by hGH... - Novel mfgl2 antisense plasmid inhibits murine fgl2 expression and ameliorates murine hepatitis virus type 3-induced fulminant hepatitis in BALB/cJ miceChuanlong Zhu
Laboratory of Infectious Immunology, Department of Infectious Disease, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
Hum Gene Ther 17:589-600. 2006.... - Global genechip profiling to identify genes responsive to p53-induced growth arrest and apoptosis in human lung carcinoma cellsMegan Robinson
Departments of Molecular Sciences and Technologies Pfizer Global Research and Development Ann Arbor Laboratories Ann Arbor, Michigan USA
Cancer Biol Ther 2:406-15. 2003..Further characterization of these genes will lead to a better understanding of the mechanism of p53 action and p53 regulation of other signaling pathways. It will also provide novel cancer drug targets for further validation... - HIV-1 Tat depresses DNA-PK(CS) expression and DNA repair, and sensitizes cells to ionizing radiationYi Sun
Department of Radiation Toxicology and Oncology, Beijing Institute of Radiation Medicine, Beijing, People s Republic of China
Int J Radiat Oncol Biol Phys 65:842-50. 2006..Here we explored the effects of the HIV-1 Tat protein on cellular responses to ionizing radiation... - Gene expression changes induced by green tea polyphenol (-)-epigallocatechin-3-gallate in human bronchial epithelial 21BES cells analyzed by DNA microarrayRagini Vittal
Susan Lehman Cullman Laboratory for Cancer Research, Department of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers University, State University of New Jersey, 164 Frelinghuysen Road, Piscataway, NJ 08854, USA
Mol Cancer Ther 3:1091-9. 2004..The elucidation of gene expression changes between H2O2-dependent and H2O2-independent responses helps us better understand the cancer chemopreventive and anticancer actions of EGCG... - Combinatorial interactions of p53, activating protein-2, and YB-1 with a single enhancer element regulate gelatinase A expression in neoplastic cellsPeter R Mertens
Department of Nephrology and Immunology, Medical Clinic II, RWTH Aachen, Pauwelsstrasse 30, Germany
J Biol Chem 277:24875-82. 2002.... - An essential role for orexins in emergence from general anesthesiaMax B Kelz
Department of Anesthesiology and Critical Care, Mahoney Institute for Neurological Sciences, Center for Sleep and Respiratory Neurobiology, University of Pennsylvania, Philadelphia, PA 19104, USA
Proc Natl Acad Sci U S A 105:1309-14. 2008..These findings support the concept that emergence depends, in part, on recruitment and stabilization of wake-active regions of brain... - Effect of hepatitis C virus nonstructural protein NS3 on proliferation and MAPK phosphorylation of normal hepatocyte lineDe Yun Feng
Department of Pathology, College of Basic Medicine, Central South University, Changsha 410078, Hunan Province, China
World J Gastroenterol 11:2157-61. 2005..To study the effect of hepatitis C virus nonstructural region 3 (HCV NS3) protein on proliferation and transformation of normal human liver cell line... - Possible role of direct Rac1-Rab7 interaction in ruffled border formation of osteoclastsYi Sun
Department of Anatomy, Institute of Biomedicine, University of Turku, Finland
J Biol Chem 280:32356-61. 2005.... - Signaling of human ciliary neurotrophic factor (CNTF) revisited. The interleukin-6 receptor can serve as an alpha-receptor for CTNFBjörn Schuster
Biochemisches Institut, Christian Albrechts Universitat zu Kiel, Olshausenstr 40, D 24098 Kiel, Germany
J Biol Chem 278:9528-35. 2003..Engineering a CNTFR-specific human CNTF variant may therefore be a prerequisite to improving the safety profile of CNTF... - Smad4 inhibits tumor growth by inducing apoptosis in estrogen receptor-alpha-positive breast cancer cellsQingnan Li
Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama 35294 0019, USA
J Biol Chem 280:27022-8. 2005..Smad4-induced apoptosis in ERalpha-positive breast cancer cells may explain the invasive nature of ERalpha-negative breast tumors, thereby providing a potential target for breast cancer intervention... - Inhibitory effect of the rhizomes of Alpinia officinarum on TPA-induced inflammation and tumor promotion in two-stage carcinogenesis in mouse skinKen Yasukawa
Nat Med (Tokyo) 62:374-8. 2008..These compounds (1-7) tested showed marked anti-inflammatory effects, with a 50% inhibitory dose of 0.8-2.7 micromol/ear...