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How dna become cancerous

Zhe Wang
Biology research has entered into big data era. Systems biology approaches therefore become the powerful tools to obtain the whole landscape of how cell separate, grow, and resist the stresses. Fission yeast Schizosaccharomyces pombe is wonderful unicellular eukaryote model, especially studying its division and metabolism can facilitate to understanding the molecular mechanism of cancer and discovering anticancer agents. In this perspective, we discuss the recent advanced fission yeast systems biology tools, mainly focus on metabolomics profiling and metabolic modeling, protein-protein interactome and genetic interaction network, DNA sequencing and applications, and high-throughput phenotypic screening...
October 11, 2016: Current Genetics
Dalei Wu, Fraydoon Rastinejad
The mammalian basic helix-loop-helix-PER-ARNT-SIM (bHLH-PAS) transcription factors share common architectural features that include a bHLH DNA-binding domain and tandemly positioned PAS domains. The sixteen members of this family include the hypoxia-inducible factors (HIF-1α and HIF-2α), ARNT (also known as HIF-1β), CLOCK and BMAL1. Most bHLH-PAS proteins have been genetically linked to variety of diseases in humans, including cancers, metabolic syndromes and psychiatric conditions. To function as transcription factors, the bHLH-PAS proteins must form heterodimeric complexes...
October 6, 2016: Current Opinion in Structural Biology
L Hua, W Y Zheng, H Xia, P Zhou
Comprehensive multi-omics data analyses have become an important means for understanding cancer incidence and progression largely driven by the availability of high-throughput sequencing technologies for genomes, proteomes, and transcriptomes. However, how tumor cells from the site of origin of the cancer begin to grow in other sites of the body is very poorly understood. In order to examine potential connections between different cancers and to gain an insight into the metastatic process, we conducted a multi-omics data analysis using data deposited in The Cancer Genome Atlas database...
August 19, 2016: Genetics and Molecular Research: GMR
Catherine G Heath, Nicolas Viphakone, Stuart A Wilson
TRanscription and EXport (TREX) is a conserved multisubunit complex essential for embryogenesis, organogenesis and cellular differentiation throughout life. By linking transcription, mRNA processing and export together, it exerts a physiologically vital role in the gene expression pathway. In addition, this complex prevents DNA damage and regulates the cell cycle by ensuring optimal gene expression. As the extent of TREX activity in viral infections, amyotrophic lateral sclerosis and cancer emerges, the need for a greater understanding of TREX function becomes evident...
October 1, 2016: Biochemical Journal
Ryan R White, Jan Vijg
DNA double-strand breaks (DSBs) are rare, but highly toxic, lesions requiring orchestrated and conserved machinery to prevent adverse consequences, such as cell death and cancer-causing genome structural mutations. DSBs trigger the DNA damage response (DDR) that directs a cell to repair the break, undergo apoptosis, or become senescent. There is increasing evidence that the various endpoints of DSB processing by different cells and tissues are part of the aging phenotype, with each stage of the DDR associated with specific aging pathologies...
September 1, 2016: Molecular Cell
K Tominaga, T Shimamura, N Kimura, T Murayama, D Matsubara, H Kanauchi, A Niida, S Shimizu, K Nishioka, E-I Tsuji, M Yano, S Sugano, Y Shimono, H Ishii, H Saya, M Mori, K Akashi, K-I Tada, T Ogawa, A Tojo, S Miyano, N Gotoh
The transcription factor nuclear factor-κB (NF-κB) has important roles for tumorigenesis, but how it regulates cancer stem cells (CSCs) remains largely unclear. We identified insulin-like growth factor 2 (IGF2) is a key target of NF-κB activated by HER2/HER3 signaling to form tumor spheres in breast cancer cells. The IGF2 receptor, IGF1 R, was expressed at high levels in CSC-enriched populations in primary breast cancer cells. Moreover, IGF2-PI3K (IGF2-phosphatidyl inositol 3 kinase) signaling induced expression of a stemness transcription factor, inhibitor of DNA-binding 1 (ID1), and IGF2 itself...
August 22, 2016: Oncogene
Steven Henikoff
Nucleosomes function to tightly package DNA into chromosomes, but the nucleosomal landscape becomes disrupted during active processes such as replication, transcription, and repair. The realization that many proteins responsible for chromatin regulation are frequently mutated in cancer has drawn attention to chromatin dynamics; however, the basic mechanisms whereby nucleosomes are disrupted and reassembled is incompletely understood. Here, I present an overview of chromatin dynamics as has been elucidated in model organisms, in which our understanding is most advanced...
2016: Cold Spring Harbor Perspectives in Medicine
Debolina Ray, Dawit Kidane
Gut microbiota are required for host nutrition, energy balance, and regulating immune homeostasis, however, in some cases, this mutually beneficial relationship becomes twisted (dysbiosis), and the gut flora can incite pathological disorders including colon cancer. Microbial dysbiosis promotes the release of bacterial genotoxins, metabolites, and causes chronic inflammation, which promote oxidative DNA damage. Oxidized DNA base lesions are removed by base excision repair (BER), however, the role of this altered function of BER, as well as microbiota-mediated genomic instability and colon cancer development, is still poorly understood...
2016: Journal of Cancer
H Dai, J L Ellis, D A Sinclair, B P Hubbard
The NAD(+)-dependent deacetylase SIRT1 plays key roles in numerous cellular processes including DNA repair, gene transcription, cell differentiation, and metabolism. Overexpression of SIRT1 protects against a number of age-related diseases including diabetes, cancer, and Alzheimer's disease. Moreover, overexpression of SIRT1 in the murine brain extends lifespan. A number of small-molecule sirtuin-activating compounds (STACs) that increase SIRT1 activity in vitro and in cells have been developed. While the mechanism for how these compounds act on SIRT1 was once controversial, it is becoming increasingly clear that they directly interact with SIRT1 and enhance its activity through an allosteric mechanism...
2016: Methods in Enzymology
Hernando Lopez-Bertoni, John Laterra
Cancer stem cells and their relatively differentiated progenitors coexist in dynamic equilibrium and are subject to bidirectional conversion. We recently showed that reprogramming transcription factors induce glioblastoma cells to become stem-like and tumor propagating via a mechanism involving changes in global DNA methylation and downregulation of miRNAs.
July 2015: Molecular & Cellular Oncology
Heidi S Bretscher, Donald T Fox
Conserved DNA-damage responses (DDRs) sense genome damage and prevent mitosis of broken chromosomes. How cells lacking DDRs cope with broken chromosomes during mitosis is poorly understood. DDRs are frequently inactivated in cells with extra genomes (polyploidy), suggesting that study of polyploidy can reveal how cells with impaired DDRs/genome damage continue dividing. Here, we show that continued division and normal organ development occurs in polyploid, DDR-impaired Drosophila papillar cells. As papillar cells become polyploid, they naturally accumulate broken acentric chromosomes but do not apoptose/arrest the cell cycle...
June 6, 2016: Developmental Cell
Nicolas Malaquin, Aurélie Martinez, Francis Rodier
Cellular senescence is historically associated with cancer suppression and aging. Recently, the reach of the senescence genetic program has been extended to include the ability of senescent cells to actively participate in tissue remodelling during many physiological processes, including placental biology, embryonic patterning, wound healing, and tissue stress responses caused by cancer therapy. Besides growth arrest, a significant feature of senescent cells is their ability to modify their immediate microenvironment using a senescence-associated (SA) secretome, commonly termed the SA secretory phenotype (SASP)...
September 2016: Experimental Gerontology
Jun Li, Gerben Duns, Helga Westers, Rolf Sijmons, Anke van den Berg, Klaas Kok
In the past decade important progress has been made in our understanding of the epigenetic regulatory machinery. It has become clear that genetic aberrations in multiple epigenetic modifier proteins are associated with various types of cancer. Moreover, targeting the epigenome has emerged as a novel tool to treat cancer patients. Recently, the first drugs have been reported that specifically target SETD2-negative tumors. In this review we discuss the studies on the associated protein, Set domain containing 2 (SETD2), a histone modifier for which mutations have only recently been associated with cancer development...
May 14, 2016: Oncotarget
Min Li, Yilun Liu
Mammalian topoisomerase 1 (TOP1) is an essential enzyme for normal development. TOP1 relaxes supercoiled DNA to remove helical constraints that can otherwise hinder DNA replication and transcription and thus block cell growth. Unfortunately, this exact activity can covalently trap TOP1 on the DNA that could lead to cell death or mutagenesis, a precursor for tumorigenesis. It is therefore important for cells to find a proper balance between the utilization of the TOP1 catalytic activity to maintain DNA topology and the risk of accumulating the toxic DNA damages due to TOP1 trapping that prevents normal cell growth...
June 2016: Genomics, Proteomics & Bioinformatics
Yelena Chernyavskaya, Brandon Kent, Kirsten C Sadler
The cancer epigenome is fundamentally different than that of normal cells. How these differences arise in and contribute to carcinogenesis is not known, and studies using model organisms such as zebrafish provide an opportunity to address these important questions. Modifications of histones and DNA comprise the complex epigenome, and these influence chromatin structure, genome stability and gene expression, all of which are fundamental to the cellular changes that cause cancer. The cancer genome atlas covers the wide spectrum of genetic changes associated with nearly every cancer type, however, this catalog is currently uni-dimensional...
2016: Advances in Experimental Medicine and Biology
Yan-Ruide Li, Wan-Xi Yang
Myosin is a kind of actin-based motor protein. As the crucial functions of myosin during tumorigenesis have become increasingly apparent, the profile of myosin in the field of cancer research has also been growing. Eighteen distinct classes of myosins have been discovered in the past twenty years and constitute a diverse superfamily. Various myosins share similar structures. They all convert energy from ATP hydrolysis to exert mechanical stress upon interactions with microfilaments. Ongoing research is increasingly suggesting that at least seven kinds of myosins participate in the formation and development of cancer...
April 19, 2016: Oncotarget
Lijun Cheng, Bryan P Schneider, Lang Li
BACKGROUND: Cancer has been extensively characterized on the basis of genomics. The integration of genetic information about cancers with data on how the cancers respond to target based therapy to help to optimum cancer treatment. OBJECTIVE: The increasing usage of sequencing technology in cancer research and clinical practice has enormously advanced our understanding of cancer mechanisms. The cancer precision medicine is becoming a reality. Although off-label drug usage is a common practice in treating cancer, it suffers from the lack of knowledge base for proper cancer drug selections...
July 2016: Journal of the American Medical Informatics Association: JAMIA
Fred Zepp
While many of the currently available vaccines have been developed empirically, with limited understanding on how they activate the immune system and elicit protective immunity, the recent progress in basic sciences like immunology, microbiology, genetics, and molecular biology has fostered our understanding on the interaction of microorganisms with the human immune system. In consequence, modern vaccine development strongly builds on the precise knowledge of the biology of microbial pathogens, their interaction with the human immune system, as well as their capacity to counteract and evade innate and adaptive immune mechanisms...
2016: Methods in Molecular Biology
Foad J Rouhani, Serena Nik-Zainal, Arthur Wuster, Yilong Li, Nathalie Conte, Hiroko Koike-Yusa, Natsuhiko Kumasaka, Ludovic Vallier, Kosuke Yusa, Allan Bradley
The accuracy of replicating the genetic code is fundamental. DNA repair mechanisms protect the fidelity of the genome ensuring a low error rate between generations. This sustains the similarity of individuals whilst providing a repertoire of variants for evolution. The mutation rate in the human genome has recently been measured to be 50-70 de novo single nucleotide variants (SNVs) between generations. During development mutations accumulate in somatic cells so that an organism is a mosaic. However, variation within a tissue and between tissues has not been analysed...
April 2016: PLoS Genetics
Yafei Dai, Lujuan Wang, Jingqun Tang, Pengfei Cao, Zhaohui Luo, Jun Sun, Abraha Kiflu, Buqing Sai, Meili Zhang, Fan Wang, Guiyuan Li, Juanjuan Xiang
Cancer dormancy is a stage in tumor progression in which residual disease remains occult and asymptomatic for a prolonged period. Cancer cell dormancy is the main cause of cancer recurrence and failure of therapy. However, cancer dormancy is poorly characterized and the mechanisms of how cancer cells develop dormancy and relapse remain elusive. In this study, 5- fluorouracil (5-FU) was used to induce cancer cell dormancy. We found that cancer cells escape the cytotoxicity of 5-FU by becoming "dormant". After exposure to 5-FU, residual non-small cell lung cancer (NSCLC) cells underwent epithelial-mesenchymal transition (EMT), followed by mesenchymal-epithelial transition (MET)...
May 3, 2016: Oncotarget
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