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Search Results: 1 - 10 of 1291 matches for " Guangchao Sui "
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The Regulation of YY1 in Tumorigenesis and its Targeting Potential in Cancer Therapy
Guangchao Sui
Molecular and Cellular Pharmacology , 2009,
Abstract: Yin Yang 1 (YY1) is a multifunctional protein and regulates various processes of development and differentiation. Increasing evidence indicates an essential role of YY1 in tumorigenesis. As a transcription factor, YY1 regulates the expression of numerous genes that are mostly involved in cancers. YY1 can either activate or repress the target genes, depending on the cofactors that it recruits. Importantly, most studies to date suggest a proliferative or oncogenic role of YY1 in cancer development. Meanwhile, overexpression of YY1 has been observed in different types of cancers and YY1 has been proposed as a potential prognostic marker of these cancers. A reasonable hypothesis is that upregulated YY1 leads to unbalanced expression of its target genes and in turn initiates or arguments tumorigenesis. Ample studies indicate that YY1 exerts broad regulation in various epigenetic events, especially histone acetylation and methylation. Since most cancers exhibit deregulated epigenetics, overexpressed YY1 may contribute to these aberrant epigenetic statuses in cancer cells. The epigenetic processes regulated by YY1 are reversible. Therefore, it is possible that targeting YY1 may adjust various deregulated epigenetic events in cancer cells, restore the normal epigenetic conditions and consequently block cancer development. This review summarizes cancer-related studies of YY1 and discusses the potential of YY1 as a target of cancer therapy.
Noncoding RNA in Oncogenesis: A New Era of Identifying Key Players
Guorui Deng,Guangchao Sui
International Journal of Molecular Sciences , 2013, DOI: 10.3390/ijms140918319
Abstract: New discoveries and accelerating progresses in the field of noncoding RNAs (ncRNAs) continuously challenges our deep-rooted doctrines in biology and sometimes our imagination. A growing body of evidence indicates that ncRNAs are important players in oncogenesis. While a stunning list of ncRNAs has been discovered, only a small portion of them has been examined for their biological activities and very few have been characterized for the molecular mechanisms of their action. To date, ncRNAs have been shown to regulate a wide range of biological processes, including chromatin remodeling, gene transcription, mRNA translation and protein function. Dysregulation of ncRNAs contributes to the pathogenesis of a variety of cancers and aberrant ncRNA expression has a high potential to be prognostic in some cancers. Thus, a new cancer research era has begun to identify novel key players of ncRNAs in oncogenesis. In this review, we will first discuss the function and regulation of miRNAs, especially focusing on the interplay between miRNAs and several key cancer genes, including p53, PTEN and c-Myc. We will then summarize the research of long ncRNAs (lncRNAs) in cancers. In this part, we will discuss the lncRNAs in four categories based on their activities, including regulating gene expression, acting as miRNA decoys, mediating mRNA translation, and modulating protein activities. At the end, we will also discuss recently unraveled activities of circular RNAs (circRNAs).
Radiation-Induced c-Jun Activation Depends on MEK1-ERK1/2 Signaling Pathway in Microglial Cells
Zhiyong Deng, Guangchao Sui, Paulo Mottin Rosa, Weiling Zhao
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0036739
Abstract: Radiation-induced normal brain injury is associated with acute and/or chronic inflammatory responses, and has been a major concern in radiotherapy. Recent studies suggest that microglial activation is a potential contributor to chronic inflammatory responses following irradiation; however, the molecular mechanism underlying the response of microglia to radiation is poorly understood. c-Jun, a component of AP-1 transcription factors, potentially regulates neural cell death and neuroinflammation. We observed a rapid increase in phosphorylation of N-terminal c-Jun (on serine 63 and 73) and MAPK kinases ERK1/2, but not JNKs, in irradiated murine microglial BV2 cells. Radiation-induced c-Jun phosphorylation is dependent on the canonical MEK-ERK signaling pathway and required for both ERK1 and ERK2 function. ERK1/2 directly interact with c-Jun in vitro and in cells; meanwhile, the JNK binding domain on c-Jun is not required for its interaction with ERK kinases. Radiation-induced reactive oxygen species (ROS) potentially contribute to c-Jun phosphorylation through activating the ERK pathway. Radiation stimulates c-Jun transcriptional activity and upregulates c-Jun-regulated proinflammatory genes, such as tumor necrosis factor-α, interleukin-1β, and cyclooxygenase-2. Pharmacologic blockade of the ERK signaling pathway interferes with c-Jun activity and inhibits radiation-stimulated expression of c-Jun target genes. Overall, our study reveals that the MEK-ERK1/2 signaling pathway, but not the JNK pathway, contributes to the c-Jun-dependent microglial inflammatory response following irradiation.
Dmp1α Inhibits HER2/neu-Induced Mammary Tumorigenesis
Elizabeth A. Fry, Pankaj Taneja, Dejan Maglic, Sinan Zhu, Guangchao Sui, Kazushi Inoue
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0077870
Abstract: Our recent study shows a pivotal role of Dmp1 in quenching hyperproliferative signals from HER2 to the Arf-p53 pathway as a safety mechanism to prevent breast carcinogenesis. To directly demonstrate the role of Dmp1 in preventing HER2/neu-driven oncogenic transformation, we established Flag-Dmp1α transgenic mice (MDTG) under the control of the mouse mammary tumor virus (MMTV) promoter. The mice were viable but exhibited poorly developed mammary glands with markedly reduced milk production; thus more than half of parous females were unable to support the lives of new born pups. The mammary glands of the MDTG mice had very low Ki-67 expression but high levels of Arf, Ink4a, p53, and p21Cip1, markers of senescence and accelerated aging. In all strains of generated MDTG;neu mice, tumor development was significantly delayed with decreased tumor weight. Tumors from MDTG;neu mice expressed Flag-Dmp1α and Ki-67 in a mutually exclusive fashion indicating that transgenic Dmp1α prevented tumor growth in vivo. Genomic DNA analyses showed that the Dmp1α transgene was partially lost in half of the MDTG;neu tumors, and Western blot analyses showed Dmp1α protein downregulation in 80% of the cases. Our data demonstrate critical roles of Dmp1 in preventing mammary tumorigenesis and raise the possibility of treating breast cancer by restoring Dmp1α expression.
Positive and Negative Regulation of Prostate Stem Cell Antigen Expression by Yin Yang 1 in Prostate Epithelial Cell Lines
Shuai Tang, Meenu Mishra, Donna P. Frazier, Miranda L. Moore, Kazushi Inoue, Rajendar Deora, Guangchao Sui, Purnima Dubey
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035570
Abstract: Prostate cancer is influenced by epigenetic modification of genes involved in cancer development and progression. Increased expression of Prostate Stem Cell Antigen (PSCA) is correlated with development of malignant human prostate cancer, while studies in mouse models suggest that decreased PSCA levels promote prostate cancer metastasis. These studies suggest that PSCA has context-dependent functions, and could be differentially regulated during tumor progression. In the present study, we identified the multi-functional transcription factor Yin Yang 1 (YY1) as a modulator of PSCA expression in prostate epithelial cell lines. Increased YY1 levels are observed in prostatic intraepithelial neoplasia (PIN) and advanced disease. We show that androgen-mediated up-regulation of PSCA in prostate epithelial cell lines is dependent on YY1. We identified two direct YY1 binding sites within the PSCA promoter, and showed that the upstream site inhibited, while the downstream site, proximal to the androgen-responsive element, stimulated PSCA promoter activity. Thus, changes in PSCA expression levels in prostate cancer may at least partly be affected by cellular levels of YY1. Our results also suggest multiple roles for YY1 in prostate cancer which may contribute to disease progression by modulation of genes such as PSCA.
MicroRNA-101 negatively regulates Ezh2 and its expression is modulated by androgen receptor and HIF-1α/HIF-1β
Paul Cao, Zhiyong Deng, Meimei Wan, Weiwei Huang, Scott D Cramer, Jianfeng Xu, Ming Lei, Guangchao Sui
Molecular Cancer , 2010, DOI: 10.1186/1476-4598-9-108
Abstract: In our reporter assays, both miR-101 and miR-26a inhibit the expression of a reporter construct containing the 3'-UTR of Ezh2. When ectopically expressed in PC-3, DU145 and LNCaP cells, miR-101 inhibits endogenous Ezh2 expression in all three cell lines, while miR-26a only decreases Ezh2 in DU145. Ectopic miR-101 reduces the invasion ability of PC-3 cells, while restored Ezh2 expression rescues the invasiveness of PC-3 cells. Similarly, miR-101 also inhibits cell invasion and migration of DU145 and LNCaP cells, respectively. Interestingly, ectopic miR-101 exhibits differential effects on the proliferation of PC-3, DU-145 and LNCaP cells and also causes morphological changes of LNCaP cells. In addition, the expression of miR-101 is regulated by androgen receptor and HIF-1α/HIF-1β. While HIF-1α/HIF-1β induced by deferoxamine mesylate (DFO) decreases miR-101 levels, the overall effects of R-1881 on miR-101 expression are stimulatory.This study indicates that miR-101 targets Ezh2 and decreases the invasiveness of PCa cells, suggesting that miR-101 introduction is a potential therapeutic strategy to combat PCa. MiR-101 differentially regulates prostate cell proliferation. Meanwhile, the expression of miR-101 is also modulated at different physiological conditions, such as androgen stimulation and HIF-1α/HIF-1β induction.Enhancer of zeste homolog 2 (Ezh2) is a member of the polycomb group (PcG) protein family involved in suppressing gene expression through remodeling chromatin [1]. As a histone methyltransferase, Ezh2 catalyzes histone H3 lysine 27 (H3-K27) trimethylation [2], which is a hallmark of gene silencing [3]. Ezh2 is an important component of the polycomb repressive complex 2 (PRC2) and is required in maintaining gene silencing. The association of Ezh2 with other PcG proteins is essential to its methyltransferase function, since the pharmacologic disruption of PRC2 inhibits the methylation of H3-K27 [4]. Ezh2 needs to be recruited by DNA binding proteins, such a
BAD Dephosphorylation and Decreased Expression of MCL-1 Induce Rapid Apoptosis in Prostate Cancer Cells
Dana Yancey, Kyle C. Nelson, Daniele Baiz, Sazzad Hassan, Anabel Flores, Ashok Pullikuth, Yelena Karpova, Linara Axanova, Victoria Moore, Guangchao Sui, George Kulik
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0074561
Abstract: PTEN loss and constitutive activation of the PI3K signaling pathway have been associated with advanced androgen-independent prostate cancer. PTEN-deficient prostate cancer C42Luc cells survive in serum-free media and show relative resistance to apoptosis even in the presence of the PI3K inhibitor ZSTK474. Yet, when ZSTK474 is combined with the translation inhibitor cycloheximide, C42Luc cells undergo apoptosis within 6 hours. We identified dephosphorylation of BAD (Bcl2-associated death promoter) as a main apoptosis-regulatory molecule downstream from PI3K, and loss of MCL-1 (Myeloid cell leukemia -1) as a major target of cycloheximide. The combination of MCL-1 knockdown and expression of phosphorylation-deficient mutant BAD2SA is sufficient to trigger rapid apoptosis in prostate cancer cells. These results establish the mechanism for the synergistic induction of apoptosis by the combination of a PI3K inhibitor and of a protein synthesis inhibitor in PTEN-deficient prostate cancer cells.
Literature Analysis of Innovation Diffusion  [PDF]
Ying Li, Mengqing Sui
Technology and Investment (TI) , 2011, DOI: 10.4236/ti.2011.23016
Abstract: The theory of innovation diffusion has become increasingly complex and multifaceted in recent years. It has been used in consumer durables, services, pharmaceutical industry and other industry research. In this paper, we use literature analysis to study the development of innovation diffusion theory, searching related literatures from Elsevier, EBSCO, Emerald, Scopus and ISI databases published between 1990 and 2010. From these literatures, we analyze the number of literatures, journal distribution, core authors, as well as the main research directions. Then, we get many conclusions which are useful for the future research of innovation diffusion.
One Sound and Complete R-Calculus with Pseudo-Subtheory Minimal Change Property  [PDF]
Wei Li, Yuefei Sui
Journal of Computer and Communications (JCC) , 2013, DOI: 10.4236/jcc.2013.15004
Abstract:

The AGM axiom system is for the belief revision (revision by a single belief), and the DP axiom system is for the iterated revision (revision by a finite sequence of beliefs). Li [1] gave an R-calculus for R-configurations Δ|Γ, where Δ is a set of atomic formulas or the negations of atomic formulas, and Γ is a finite set of formulas. In propositional logic programs, one R-calculus N will be given in this paper, such that N is sound and complete with respect to operator s(Δ,t), where s(Δ,t)is a pseudo-theory minimal change of t by Δ.

The Sound and Complete R-Calculi with Respect to Pseudo-Revision and Pre-Revision  [PDF]
Wei Li, Yuefei Sui
International Journal of Intelligence Science (IJIS) , 2013, DOI: 10.4236/ijis.2013.32012
Abstract: The AGM postulates ([1]) are for the belief revision (revision by a single belief), and the DP postulates ([2]) are for the iterated revision (revision by a finite sequence of beliefs). Li [3] gave an R-calculus for R-configurations |Γ, where Δ is a set of literals, and Γ is a finite set of formulas. We shall give two R-calculi such that for any consistent set Γ and finite consistent set of formulas in the propositional logic, in one calculus, there is a pseudo-revision Θ of Γ by Δ such that \"\" is provable and \"\" and in another calculus, there is a pre-revision Ξ
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