Critical Reviews in Eukaryotic Gene Expression (CRIT REV EUKAR GENE)

Publications in this journal

• Article: Role of cancer-related inflammation in esophageal cancer.

  Mingxin Zhang, Suna Zhou, Lingmin Zhang, Wenguang Ye, Qinsheng Wen, Jingjie Wang
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  ABSTRACT: Esophageal cancer (EC) is the ninth most common malignancy with a poor prognosis. It is clear that improvements need to be made to reveal the exact molecular mechanisms of EC. Cancer-related inflammation (CRI) recently has been proposed as a major physiological hallmark of malignancy and has important value in diagnosis, treatment, and prognosis. But the role of CRI in EC has remained unclear. In this review, we focus primarily on the function of key mediators of CRI in EC, including transcription factors, chemokines, cytokines, reactive oxygen species, COX-2, and specific microRNAs. Through a comprehensive analysis, we try to reveal the interaction between CRI and EC, providing novel preventive, diagnostic, and therapeutic strategies to reduce the health burden of EC.
  Critical Reviews in Eukaryotic Gene Expression 01/2013; 23(1):27-35.
• Article: Brucella virulence mechanisms and implications in novel vaccines and drugs.

  Guangjun Gao, Yufei Wang, Zeliang Chen, Xingran Xu, Jie Xu
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  ABSTRACT: Brucellosis, an infection caused by Brucella spp., is a common zoonosis in many parts of world. Human chronic infection is successfully established through contact with infected animals or their dirty products. The capacity of establishing and maintaining this persistent infection in the phagosomal compartment of host macro-phages is critical to their ability to produce chronic infections in their mammalian hosts. Bacterial virulence mechanisms play an important role in regulating during the infectious process, both to optimize the functioning of the virulence factors in promoting survival and thwarting host defenses and to produce an effective immune response against these virulence components. The availability of the genomic sequences and molecular strategies such as gene mutant technique provide an opportunity to identify the virulence mechanisms of Brucella. It will greatly accelerate our understanding of the infection of this pathogen and give us more clues to exploit new vaccines and drugs.
  Critical Reviews in Eukaryotic Gene Expression 01/2013; 23(1):49-64.
• Article: The Nuclear Import Receptor Kpnβ1 and Its Potential as an AntiCancer Therapeutic Target.

  Pauline J van der Watt, Catherine L Stowell, Virna D Leaner
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  ABSTRACT: Many proteins require transport across the nuclear envelope, the physical barrier separating the nucleus from the cytoplasm. Karyopherin β (Kpnβ1) proteins are the major nuclear receptor proteins in the cell that cargo proteins across the nuclear envelope, allowing them to enter and exit the cell nucleus. Karyopherin β1, a major nuclear import receptor, plays an integral role in importing transcription factors, cell signaling proteins, cell cycle proteins, and so forth, into the nucleus, thus playing a crucial role in maintaining normal cell homeostasis. However, cancer cells appear to differentially regulate the expression of the Karyopherin β proteins, presumably in order to maintain increased nuclear transport rates, thus implicating this protein family as a target for cancer therapy. The role of Kpnβ1 in cancer is only now being elucidated, and recent work points to its potential usefulness as an anti-cancer target.
  Critical Reviews in Eukaryotic Gene Expression 01/2013; 23(1):1-10.
• Article: The role of cathepsins in osteoimmunology.

  Peter Pietschmann, Ursula Foger-Samwald, Wolfgang Sipos, Martina Rauner
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  ABSTRACT: Cathepsins are proteases comprising two small groups of serine and aspartic cathepsins and a large group of lysosomal cysteine cathepsins. Most of them are ubiquitously expressed throughout human tissues but some of them display a more restricted expression pattern and are involved in explicit tasks such as collagen degradation in the process of bone and cartilage destruction or degradation of invariant chain peptides in the process of antigen processing and presentation. In addition to the aforementioned functions, cathepsins have been shown to play a critical role in the pathogenesis of osteoimmunological diseases involving mutual interactions between skeletal and immunological functions. The most convincing evidence that cathepsins participate in the pathogenesis of osteoimmunological disorders exists for cathepsins K and S. Therefore, this review focuses on recent advances in understanding the role of cathepsins K and S in osteoimmunology and highlights the progress that has been made in targeting cathepsins to treat diseases related to the skeletal or immune system.
  Critical Reviews in Eukaryotic Gene Expression 01/2013; 23(1):11-26.
• Article: Weight change patterns and breast cancer risk: a brief review and analysis.

  Mary C Playdon, Shawna B Matthews, Henry J Thompson
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  ABSTRACT: Body weight change is defined as one or more periods of weight gain or weight loss that can vary in terms of magnitude, timeframe over which the change(s) occurs, and the number of times the pattern changes. Epidemiological and clinical data provide evidence of increased lifetime risk for breast cancer due to adult weight gain and a reduction of risk with weight loss. These findings parallel the majority of preclinical carcinogenesis experiments in which caloric intake in excess of basal metabolic requirements in rodents permits the development of cancer in proportion to the level of caloric intake. Dieting has been unsuccessful in reducing cancer risk unless a lower body weight was maintained at the end of weight change. Based on this evidence, it is recommended that consideration be given to the inclusion of the following recommendations in clinical practice guidelines for managing lifetime risk for breast cancer: (1) maintain adult body mass index in the desirable range (18.5-24.9 kg/m2) by preventing adult weight gain in both pre- and postmenopausal women, and (2) actively monitor BMI and, when BMI is above the defined ideal range, prescribe corrective lifestyle changes until body weight returns to the target range.
  Critical Reviews in Eukaryotic Gene Expression 01/2013; 23(2):159-69.
• Article: Important biology events and pathways in Brucella infection and implications for novel antibiotic drug targets.

  Guangjun Gao, Jie Xu
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  ABSTRACT: Brucellosis caused by Brucella spp. is a common zoonosis in many parts of the world. Humans are infected through contact with infected animals or their dirty products. Many mechanisms are needed for this successful infection, although the mechanisms are still unclear. Host immune response and some signaling molecules play an important role in the infection event. Bacterial pathogens operate by attacking crucial intracellular pathways or some important molecules in each of these pathways for survival in their hosts. The crucial components (molecules) of immunity or pathway play a critical role in the whole process of Brucella infection. Here we summarize the findings of the Brucella-host interactions' immune system and signaling molecular cascades involved in the TLR-initiated immune response to Brucella spp. infection. The paper serves to deepen our understanding of this complex process and to provide some clues regarding the discovery of drug targets for prevention and control.
  Critical Reviews in Eukaryotic Gene Expression 01/2013; 23(1):65-76.
• Article: The paradoxical role of nrf2 in tumor biology.

  Hui Shen, Suna Zhou, Jiansheng Wang
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  ABSTRACT: Nrf2 is used as a cell protector by mediating many downstream genes which express phase II detoxifying and antioxidant enzymes. Recently, large numbers of experiments have shown Nrf2 and its downstream genes are found to be overexpressed in many human tumors. Numerous evidences unveil that Nrf2 protects the normal cells while promoting the malignant tumor's progression. The paradoxical role of Nrf2 has not been clearly elucidated before. Here, we review the suppressor or oncogene roles of Nrf2 in different stages of specific tumors with respect to the newest studies. Further, we suspect that the hypoxic microenvironment around the tumors is the main crux which determines the role of Nrf2 in the tumor initiation, invasion, and metastasis. In the initiation of tumors, Nrf2 or Keap1 genes get mutations under the oxidative stress; as a result, the tumor cells obtain the advantage to growth. At the later stages, the hypoxic microenvironment around the malignant tumors has a profound influence on the character of Nrf2. Under the hypoxic microenvironment, expression of certain downstream genes of Nrf2 involved in angiogenesis are obviously elevated; other transcription factors derived from hypoxic microenvironment interact with Nrf2 and in that way promote or inhibit the invasion and metastasis.
  Critical Reviews in Eukaryotic Gene Expression 01/2013; 23(1):37-47.
• Article: Chemokines and chemokine receptors as promoters of prostate cancer growth and progression.

  Nicole Salazar, Miguel Castellan, Samir S Shirodkar, Bal L Lokeshwar
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  ABSTRACT: Prostate cancer (CaP) is estimated to be first in incidence among cancers, with more than 240,000 new cases in 2012 in the United States. Chemokines and their receptors provide survival, proliferation, and invasion characteristics to CaP cells in both primary sites of cancer and metastatic locations. The emerging data demonstrate that many chemokines and their receptors are involved in the multistep process of CaP, leading to metastasis, and, further, that these factors act cooperatively to enhance other mechanisms of tumor cell survival, growth, and metastasis. Changes of chemokine receptor cohorts may be necessary to activate tumor-promoting signals. Chemokine receptors can activate downstream effectors, such as mitogen-activated protein kinases, by complex mechanisms of ligand-dependent activation of cryptic growth factors; guanosine triphosphate-binding, protein-coupled activation of survival kinases; or transactivation of other receptors such as ErbB family members. We describe vanguard research in which more than the classic view of chemokine receptor biology was clarified. Control of chemokines and inhibition of their receptor activation may add critical tools to reduce tumor growth, especially in chemo-hormonal refractory CaP that is both currently incurable and the most aggressive form of the disease, accounting for most of the more than 28,000 annual deaths.
  Critical Reviews in Eukaryotic Gene Expression 01/2013; 23(1):77-91.
• Article: Bi-directional signaling: extracellular matrix and integrin regulation of breast tumor progression.

  Scott Gehler, Suzanne M Ponik, Kristin M Riching, Patricia J Keely
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  ABSTRACT: Cell transformation and tumor progression involve a common set of acquired capabilities, including increased proliferation, failure of cell death, self-sufficiency in growth, angiogenesis, and tumor cell invasion and metastasis. The stromal environment consists of many cell types and various extracellular matrix (ECM) proteins that support normal tissue maintenance and which have been implicated in tumor progression. Both the chemical and mechanical properties of the ECM have been shown to influence normal and malignant cell behavior. For instance, mesenchymal stem cells differentiate into specific lineages that are dependent on matrix stiffness, while tumor cells undergo changes in cell behavior and gene expression in response to matrix stiffness. ECM remodeling is implicated in tumor progression and can result in increased deposition of stromal ECM, enhanced contraction of ECM fibrils, and altered collagen alignment and ECM stiffness. Tumor cells respond to changes in ECM remodeling through altered intracellular signaling and cell cycle control that lead to enhanced proliferation, loss of normal tissue architecture, and local tumor cell migration and invasion. This review focuses on the bi-directional interplay between the mechanical properties of the ECM and integrin-mediated signal transduction events in an effort to elucidate cell behaviors during tumor progression.
  Critical Reviews in Eukaryotic Gene Expression 01/2013; 23(2):139-57.
• Article: Combined Gene Expression and DNA Occupancy Profiling as a Strategy to Identify Therapeutic Target(s) in t(8;21) Acute Myeloid Leukemia.

  Miao-Chia Lo, Luke F Peterson
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  ABSTRACT: Microarray technology has contributed valuable information to gene expression signatures of leukemia and other types of cancers and helped to identify biological markers and potential therapeutic targets for treating these diseases. Acute myeloid leukemia (AML) is often caused by aberrant fusion transcription factors resulting from chromosomal translocations, and the dysregulated genes detected by microarray include both direct and indirect targets of the oncogenic transcription factors. The ChIP-chip technology enables the identification of direct targets of a transcription factor based on its promoter occupancy and cellular context. Using AML1-ETO9a-induced AML as a cancer model and using a combined gene expression and promoter occupancy profiling approach, we recently identified CD45 as a direct down-regulated target of t(8;21) fusion proteins. This finding subsequently led us to discover the enhanced Janus activated kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway, which is negatively regulated by CD45, in t(8;21) AML. This review summarizes the background of t(8;21) leukemia, structural features of the translocation fusion proteins, and the merits of combining gene discovery technologies for the identification of therapeutic targets in t(8;21) leukemia.
  Critical Reviews in Eukaryotic Gene Expression 01/2013; 23(2):103-13.
• Article: Detection of RNA viruses: current technologies and future perspectives.

  Lakshmi N Cella, Daniel Blackstock, Marylynn A Yates, Ashok Mulchandani, Wilfred Chen
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  ABSTRACT: RNA viruses constitute one of the major classes of pathogenic organisms causing human diseases, with varying degrees of severity. This review summarizes the conventional and emerging technologies that are available for the detection of these organisms. Cell culture-based techniques for viral detection have been popular since their inception and continue to be the gold standard against which all other techniques. Over many years, these techniques have undergone some radical changes, reducing the total time needed for detection and improving sensitivity, although even with their reliability and improved features they are being slowly replaced by nucleic acid-based technologies. These molecular detection techniques have revolutionized the area of viral detection by their high sensitivity, selectivity, and short detection time. The majority of nucleic acid-based techniques depend on amplifying viral RNA; however, there are some newer emerging techniques that detect viral RNA in live cells using various configurations of florescent probes. In addition, nucleic acid-based technology has made it possible for multiviral detection with either multiplex polymerase chain reaction assays or microarrays. Every technique described in this review has its own unique abilities, making them indispensable for viral detection. However, we believe that nucleic acid-based technologies will find widespread use after being standardized, limiting other technologies to very specific uses.
  Critical Reviews in Eukaryotic Gene Expression 01/2013; 23(2):125-37.
• Article: Association Between CD14 Gene Polymorphism and Periodontitis: A Meta-Analysis.

  Jingjing Zheng, Tiezhou Hou, Ling Gao, Cuiyan Wu, Pan Wang, Yan Wen, Xiong Guo
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  ABSTRACT: This meta-analysis aimed to analyze the association between CD14 C-159T and C-260T polymorphisms and periodontitis risks because previous results have been conflicting. We used 12 eligible case-control studies involving 1435 cases and 1446 controls to evaluate this association. Compared with the common CD14 C-159T and C-260T genotypes, there was no significant association of T alleles and the CT/TT genotypes polymorphism with periodontitis risk (odds ratio [OR], 1.03; 95% confidence interval [CI], 0.83-1.27 for C vs. T; OR, 1.07; 95% CI, 0.83-1.38 for CT/TT vs. CC). A similar result was found in a subgroup analysis by ethnicity and periodontitis type. An enhanced risk for periodontitis was demonstrated in the comparison of subjects carrying the CT genotype versus CC homozygotes (overall OR, 1.681; 95% CI, 1.048-2.695; P for heterogeneity = 0.367; I2 = 2.00%) for the C-260T genotype. Our meta-analysis revealed that the 2 common CD14 polymorphisms, C-159T and C-260T, have no association with the likelihood of periodontitis. In subgroup analysis by ethnicity and periodontitis type, the results also did not show any association. The effect of genetic networks and their mutual interactions in the CD14 signaling pathway on susceptibility to periodontitis need to be studied further.
  Critical Reviews in Eukaryotic Gene Expression 01/2013; 23(2):115-23.
• Article: ANP-NPRA Signaling Pathway-A Potential Therapeutic Target for the Treatment of Malignancy.

  Zhilong Zhao, Jia Zhang, Min Li, Ya Yang, Kai Sun, Jiansheng Wang
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  ABSTRACT: It was well established that the atrial natriuretic peptide (ANP)/natriuretic peptide receptor-A (NPRA) signaling pathway controls natriuretic, diuretic, vasorelaxant, and anti-proliferative responses in the regulation of the human cardiovascular system by previous studies. Yet in recent years, more and more evidence has shown that the ANP/NPRA signaling pathway plays an important role in human cancer. For example, NPRA is abundantly expressed on tumorigenic mouse and human prostate cancer (PCa) cells, but not in nontumorigenic prostate epithelial cells and down-regulation of NPRA-induced apoptosis in PCa cells. Dexamethasone can increase the expression of ANP markedly, and that is the reason why dexamethasone is the cornerstone in the treatment of multiple myeloma. NPRA deficiency can substantially protect C57BL/6 mice from lung, skin, and ovarian cancers. These results strongly suggest ANP and NPRA may play an anti-cancer and carcinogenesis role, respectively, and this signaling pathway could be a more potent target for cancer therapy. In light of these new insights, this review will summarize the structures, functions, and their regulation by cell signaling, and their different impacts on tumors.
  Critical Reviews in Eukaryotic Gene Expression 01/2013; 23(2):93-101.
• Article: Biophysical and Biochemical Models of Mechanisms of Cellular Development via the Cellular Cycle in Normal Tissue, Cancerous Tissue, and Inflammatory Processes.

  Michail R Ponizovskiy
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  ABSTRACT: The significant separate biochemical discoveries of pro- and anti-apoptotic -autophagy, and -proliferative processes in normal and pathology cells were learned in detail from the point of view of biophysics, physical chemistry, and thermodynamics, which made possible the proposal that a common mechanism relates to all of these processes: intracellular balances in catabolic and anabolic processes interconnect with extracellular balances, promoting and maintaining the stability of internal medium and internal energy of cells as well as normal cell development. Nevertheless, violations to these interconnections of intracellular and extracellular balances promote pathologic processes. The study of cellular cycle mechanisms in normal cells explained the mechanisms of the maintenance of stability of the internal medium and internal energy of cells as a component of the overall stability of an organism. It explained the development of the cellular cycle as the oscillating changes in the flow of energy and substances. In addition, violations to mechanisms of the maintenance of stability of the cellular internal medium and internal energy in cancer tissue were elucidated and compared with violations of these mechanisms in inflammatory processes. All of this eliminated a lot of doubts and queries that were expressed by the authors of some experiments.
  Critical Reviews in Eukaryotic Gene Expression 01/2013; 23(2):171-93.
• Article: Insights into the Distribution and Functions of the Eukaryotic GPI-like Anchored Genes Among Mycobacterium from a Comparative Genomic Perspective.

  Wanyan Deng, Jie Zeng, Xiaohong Xiang, Jianping Xie
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  ABSTRACT: Glycosylphosphatidylinositol (GPI)-anchored proteins range from small peptides to larger antigens and fulfill a variety of cellular functions in eukaryotes. We speculated there should be such molecules in intracellular pathogens such as Mycobacterium due to their complex interplay with the host. However, no prior publications have touched this topic. To explore the existence and distribution of GPI-like molecules among Mycobacterium, we exhaustively analyzed all publicly available Mycobacterium genomes and found that the GPI-like signal sequences are prevalent among Mycobacterium, and a significant dichotomy between nonpathogenic Mycobacterium (exemplified by Mycobacterium smegmatis) and pathogenic Mycobacterium (exemplified by Mycobacterium tuberculosis), through genome-wide GPI-SOM analysis. Some well-documented anti-tuberculosis drug targets are predicted to have GPI-like anchored signals, such as KasA and atpE. Interestingly, Pro-Glu (PE) and Pro-Pro-Glu (PPE) proteins predicted to have GPI-anchoring sequence are unique to pathogenic Mycobacterium. These results can be further explored for better control measures against tuberculosis.
  Critical Reviews in Eukaryotic Gene Expression 01/2012; 22(4):299-307.
• Article: Lysosomes, growth factor activity, and carcinogenic implications.

  Marvin Melzer
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  ABSTRACT: The aim of this paper is to point out a body of literature which up to now has been largely ignored by investigators in the area of growth factors This paper will offer a response to the questions: Why is it that inhibition of endolysosomal proteases (by agents such as leupeptin, methylamine, etc.) or inhibition of endocytosis block the activities of all growth factors and carcinogens so far studied? What role therefore can endocytosis and endolysosomes (E/L) play in the signal transduction process? As will be detailed below, in many cases involving growth factors, inhibition of E/L proteases results in complete or very significant loss of growth factor activity. That is, treatment with inhibitors of E/L proteases (i.e., leupeptin, antipain methylamine, etc.) erases the normal activity of growth factors affecting systems of concern to immunologists, endocrinologists, and cardiologists. There are strong indications in the literature that suggest that in the nervous system (of obvious interest to neuroscientists) endocytosis plays a vital role in the induced proliferation of neurons as well (of interest to neurologists). This paper will explore the implications and offer an explanation for these findings. Thus this communication will travel from one growth factor to another in order to demonstrate the universality of the model offered in this paper.
  Critical Reviews in Eukaryotic Gene Expression 01/2012; 22(4):345-58.
• Article: Integrin control of tumor invasion.

  Dara S Missan, Michael Dipersio
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  ABSTRACT: Metastasis is the leading cause of death in cancer patients, and strategies to inhibit tumor cell invasion are a major focus of current efforts to develop cancer treatments. The extracellular matrix (ECM) provides both structural support and extracellular cues that regulate invasive tumor growth, and tumor-associated changes in ECM contribute to cancer progression. Integrins, the major receptors for cell adhesion to ECM, are important at every stage of cancer and occupy a critical position as transducers of chemical and mechanical signals that control tumor cell responses to ECM (i.e., outside-in signaling), as well as tumor-mediated changes to ECM that facilitate invasive growth and metastasis (i.e., inside-out signaling). Integrins are therefore attractive therapeutic targets for antagonistic agents. Here, we provide an overview of cancer-promoting functions of integrins on tumor cells, with a focus on roles in regulating cell invasion, ECM remodeling, tumor angiogenesis, and gene expression. We will also discuss how integrin functions are modulated by ECM ligands outside the cell, cytoskeletal/signaling proteins inside the cell, and other cell surface proteins. Finally, we will discuss current progress towards developing integrin antagonists for clinical use, including barriers that must still be overcome before integrins can be fully exploited as therapeutic targets.
  Critical Reviews in Eukaryotic Gene Expression 01/2012; 22(4):309-24.
• Article: Thymosin β4: a potential molecular target for tumor therapy.

  Yongtao Xiao, Yingwei Chen, Jie Wen, Weihui Yan, Kejun Zhou, Wei Cai
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  ABSTRACT: Thymosin β4 (Tβ4), a 5 kDa protein, has been demonstrated to play an important role in a variety of biological activities, such as actin sequestering, cellular motility, migration, inflammation, and damage repair. Recently, several novel findings provided compelling evidence that Tβ4 played a key role in facilitating tumor metastasis and angiogenesis. It has been found that Tβ4 expressed increasingly in a number of metastatic tumors, which was associated with an increased expression of a known angiogenic factor, vascular endothelial growth factor. Thus, Tβ4 provided a potential target of opportunity for cancer management, especially for cancer metastasis therapy.
  Critical Reviews in Eukaryotic Gene Expression 01/2012; 22(2):109-16.