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histone modification chromatin cancer

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https://www.readbyqxmd.com/read/29149419/changes-in-chromatin-state-reveal-arnt2-at-a-node-of-a-tumorigenic-transcription-factor-signature-driving-glioblastoma-cell-aggressiveness
#1
Alexandra Bogeas, Ghislaine Morvan-Dubois, Elias A El-Habr, François-Xavier Lejeune, Matthieu Defrance, Ashwin Narayanan, Klaudia Kuranda, Fanny Burel-Vandenbos, Salwa Sayd, Virgile Delaunay, Luiz G Dubois, Hugues Parrinello, Stéphanie Rialle, Sylvie Fabrega, Ahmed Idbaih, Jacques Haiech, Ivan Bièche, Thierry Virolle, Michele Goodhardt, Hervé Chneiweiss, Marie-Pierre Junier
Although a growing body of evidence indicates that phenotypic plasticity exhibited by glioblastoma cells plays a central role in tumor development and post-therapy recurrence, the master drivers of their aggressiveness remain elusive. Here we mapped the changes in active (H3K4me3) and repressive (H3K27me3) histone modifications accompanying the repression of glioblastoma stem-like cells tumorigenicity. Genes with changing histone marks delineated a network of transcription factors related to cancerous behavior, stem state, and neural development, highlighting a previously unsuspected association between repression of ARNT2 and loss of cell tumorigenicity...
November 17, 2017: Acta Neuropathologica
https://www.readbyqxmd.com/read/29142071/chromatin-histone-modifications-and-rigidity-affect-nuclear-morphology-independent-of-lamins
#2
Andrew D Stephens, Patrick Z Liu, Edward J Banigan, Luay M Almassalha, Vadim Backman, Stephen A Adam, Robert D Goldman, John F Marko
Nuclear shape and architecture influence gene localization, mechanotransduction, transcription, and cell function. Abnormal nuclear morphology and protrusions termed "blebs" are diagnostic markers for many human afflictions including heart disease, aging, progeria, and cancer. Nuclear blebs are associated with both lamin and chromatin alterations. A number of prior studies suggest that lamins dictate nuclear morphology, but the contributions of altered chromatin compaction remain unclear. We show that chromatin histone modification state dictates nuclear rigidity, and modulating it is sufficient to both induce and suppress nuclear blebs...
November 15, 2017: Molecular Biology of the Cell
https://www.readbyqxmd.com/read/29113254/epigenetic-analysis-of-fhl1-tumor-suppressor-gene-in-human-liver-cancer
#3
Jun Wang, Fang Huang, Jian Huang, Jindan Kong, Shenglan Liu, Jun Jin
Liver cancer is one of the most common types of cancer among human malignancies. Four and a half LIM domains 1 (FHL1), as a tumor suppressor gene, is frequently downregulated in multiple types of human cancer. However, the role and specific mechanisms of FHL1 as a tumor suppressor in liver cancer are poorly understood. The present study aimed to investigate the role and associated mechanisms of FHL1 in human liver cancer. The level of FHL1 mRNA in hepatocellular carcinoma (HCC) tissue specimens and cell lines derived from the human liver was determined using reverse transcription polymerase chain reaction and western blot analysis...
November 2017: Oncology Letters
https://www.readbyqxmd.com/read/29075615/pharmacologic-targeting-of-chromatin-modulators-as-therapeutics-of-acute-myeloid-leukemia
#4
REVIEW
Rui Lu, Gang Greg Wang
Acute myeloid leukemia (AML), a common hematological cancer of myeloid lineage cells, generally exhibits poor prognosis in the clinic and demands new treatment options. Recently, direct sequencing of samples from human AMLs and pre-leukemic diseases has unveiled their mutational landscapes and significantly advanced the molecular understanding of AML pathogenesis. The newly identified recurrent mutations frequently "hit" genes encoding epigenetic modulators, a wide range of chromatin-modifying enzymes and regulatory factors involved in gene expression regulation, supporting aberration of chromatin structure and epigenetic modification as a main oncogenic mechanism and cancer-initiating event...
2017: Frontiers in Oncology
https://www.readbyqxmd.com/read/29074395/epigenetics-of-malignant-melanoma
#5
REVIEW
Bruce Moran, Romina Silva, Antoinette S Perry, William M Gallagher
Patients with malignant melanoma generally have a good prognosis if the disease presents prior to metastasis. Due to progress with targeted and immunotherapies, the median survival of metastatic melanoma patients is now over 2 years. The disease is characterised by one of the highest somatic mutation rates observed amongst cancer types, with a specific mutational signature based on UV radiation damage evident. Highly prevalent mutations, such as the BRAF(V600E), in the MAPK cascade indicate truncal involvement of this pathway in the earliest stage of melanoma...
October 23, 2017: Seminars in Cancer Biology
https://www.readbyqxmd.com/read/29058709/molecular-analysis-of-prc2-recruitment-to-dna-in-chromatin-and-its-inhibition-by-rna
#6
Xueyin Wang, Richard D Paucek, Anne R Gooding, Zachary Z Brown, Eva J Ge, Tom W Muir, Thomas R Cech
Many studies have revealed pathways of epigenetic gene silencing by Polycomb repressive complex 2 (PRC2) in vivo, but understanding the underlying molecular mechanisms requires biochemistry. Here we analyze interactions of reconstituted human PRC2 with nucleosome complexes. Histone modifications, the H3K27M cancer mutation, and inclusion of JARID2 or EZH1 in the PRC2 complex have unexpectedly minor effects on PRC2-nucleosome binding. Instead, protein-free linker DNA dominates the PRC2-nucleosome interaction...
October 23, 2017: Nature Structural & Molecular Biology
https://www.readbyqxmd.com/read/29048620/dna-methylation-and-histone-modifications-as-epigenetic-regulation-in-prostate-cancer-review
#7
Maria Nowacka-Zawisza, Ewelina Wiśnik
Prostate cancer is the second most commonly diagnosed cancer in men in Poland after lung cancer and the third leading cause of cancer-related mortality after lung and colon cancer. The etiology of most cases of prostate cancer are not fully known, and therefore it is essential to search for the molecular basis of prostate cancer and markers for the early diagnosis of this type of cancer. Epigenetics deals with changes in gene expression that are not determined by changes in the DNA sequence. Epigenetic changes refer to changes in the structure of DNA, which are the result of DNA modification after replication and/or post-translational modification of proteins associated with DNA...
September 20, 2017: Oncology Reports
https://www.readbyqxmd.com/read/29045501/scaffold-dependent-histone-deacetylase-hdac-inhibitor-induced-re-equilibration-of-the-subcellular-localization-and-post-translational-modification-state-of-class-i-hdacs
#8
Thomas W Hanigan, Taha Y Taha, Shaimaa M Aboukhatwa, Jonna Frasor, Pavel A Petukhov
The mechanism of action of histone deacetylase inhibitors (HDACi) is mainly attributed to the inhibition of the deacetylase catalytic activity for their histone substrates. In this study, we analyzed the abundance of class I HDACs in the cytosolic, nuclear soluble and chromatin bound cellular fractions in breast cancer cells after HDACi treatment. We found that potent N-hydroxy propenamide-based HDACi induced a concentration dependent decrease in the HDAC1 associated with chromatin and a lasting concomitant increase in cytoplasmic HDAC1 while maintaining total protein expression...
2017: PloS One
https://www.readbyqxmd.com/read/29021135/histone-acetyltransferase-kat6a-upregulates-pi3k-akt-signaling-through-trim24-binding
#9
Deguan Lv, Feng Jia, Yanli Hou, Youzhou Sang, Angel A Alvarez, Weiwei Zhang, Wei-Qiang Gao, Bo Hu, Shi-Yuan Cheng, Jianwei Ge, Yanxin Li, Haizhong Feng
Lysine acetyltransferase KAT6A is a chromatin regulator that contributes to histone modification and cancer, but the basis of its actions are not well understood. Here, we identify a KAT6A signaling pathway that facilitates glioblastoma (GBM), where it is upregulated. KAT6A expression was associated with GBM patient survival. KAT6A silencing suppressed cell proliferation, cell migration, colony formation, and tumor development in an orthotopic mouse xenograft model system. Mechanistic investigations demonstrated that KAT6A acetylates lysine 23 of histone H3 (H3K23), which recruits the nuclear receptor binding protein TRIM24 to activate PIK3CA transcription, thereby enhancing PI3K/AKT signaling and tumorigenesis...
November 15, 2017: Cancer Research
https://www.readbyqxmd.com/read/28992434/targeting-epigenetics-in-cancer
#10
Richard L Bennett, Jonathan D Licht
Alterations of genes regulating epigenetic processes are frequently found as cancer drivers and may cause widespread alterations of DNA methylation, histone modification patterns, or chromatin structure that disrupt normal patterns of gene expression. Because of the inherent reversibility of epigenetic changes, inhibitors targeting these processes are promising anticancer strategies. Small molecules targeting epigenetic regulators have been developed recently, and clinical trials of these agents are under way for hematologic malignancies and solid tumors...
October 6, 2017: Annual Review of Pharmacology and Toxicology
https://www.readbyqxmd.com/read/28991411/structural-insights-into-the-nuclear-import-of-the-histone-acetyltransferase-mof-by-importin-%C3%AE-1
#11
Weili Zheng, Rui Wang, Xi Liu, Siyu Tian, Benqiang Yao, Ang Chen, Shikai Jin, Yong Li
The histone acetyltransferase MOF (males-absent-on-the-first) acetylates the histone H4, a modification important for many biological processes, including chromatin organization, transcriptional regulation, DNA replication, recombination and repair, as well as autophagy. Depletion of MOF induces serious consequences due to the reduction of histone acetylation, such as nuclear morphological defects and cancer. Despite the critical roles of MOF in the nucleus, the structural or functional mechanisms of the nucleocytoplasmic transport of MOF remain elusive...
October 9, 2017: Traffic
https://www.readbyqxmd.com/read/28977426/histone-h1-depletion-triggers-an-interferon-response-in-cancer-cells-via-activation-of-heterochromatic-repeats
#12
Andrea Izquierdo-Bouldstridge, Alberto Bustillos, Carles Bonet-Costa, Patricia Aribau-Miralbés, Daniel García-Gomis, Marc Dabad, Anna Esteve-Codina, Laura Pascual-Reguant, Sandra Peiró, Manel Esteller, Matthew Murtha, Lluís Millán-Ariño, Albert Jordan
Histone H1 has seven variants in human somatic cells and contributes to chromatin compaction and transcriptional regulation. Knock-down (KD) of each H1 variant in breast cancer cells results in altered gene expression and proliferation differently in a variant specific manner with H1.2 and H1.4 KDs being most deleterious. Here we show combined depletion of H1.2 and H1.4 has a strong deleterious effect resulting in a strong interferon (IFN) response, as evidenced by an up-regulation of many IFN-stimulated genes (ISGs) not seen in individual nor in other combinations of H1 variant KDs...
November 16, 2017: Nucleic Acids Research
https://www.readbyqxmd.com/read/28971591/chromatin-modification-a-novel-insight-into-braf-independent-spontaneous-melanoma
#13
Revati Darp, Craig Ceol
Chromatin modifying enzymes place and remove chemical groups on histones and DNA in a very dynamic and regulated fashion. Along with impacting the structure of chromatin by altering non-covalent interactions between nucleosomes (1), these epigenetic modifications can more directly regulate DNA-based processes including transcription, and DNA repair and replication. Aberrant activity of chromatin modifying enzymes can have profound consequences that can lead to the initiation and maintenance of various cancers (1)...
October 3, 2017: Pigment Cell & Melanoma Research
https://www.readbyqxmd.com/read/28968850/epigenetic-regulation-of-gene-expression-in-cancer-techniques-resources-and-analysis
#14
Luciane T Kagohara, Genevieve L Stein-O'Brien, Dylan Kelley, Emily Flam, Heather C Wick, Ludmila V Danilova, Hariharan Easwaran, Alexander V Favorov, Jiang Qian, Daria A Gaykalova, Elana J Fertig
Cancer is a complex disease, driven by aberrant activity in numerous signaling pathways in even individual malignant cells. Epigenetic changes are critical mediators of these functional changes that drive and maintain the malignant phenotype. Changes in DNA methylation, histone acetylation and methylation, noncoding RNAs, posttranslational modifications are all epigenetic drivers in cancer, independent of changes in the DNA sequence. These epigenetic alterations were once thought to be crucial only for the malignant phenotype maintenance...
August 11, 2017: Briefings in Functional Genomics
https://www.readbyqxmd.com/read/28967863/chromatin-accessibility-underlies-synthetic-lethality-of-swi-snf-subunits-in-arid1a-mutant-cancers
#15
Timothy W R Kelso, Devin K Porter, Maria Luisa Amaral, Maxim N Shokhirev, Christopher Benner, Diana C Hargreaves
ARID1A, a subunit of the SWI/SNF chromatin remodeling complex, is frequently mutated in cancer. Deficiency in its homolog ARID1B is synthetically lethal with ARID1A mutation. However, the functional relationship between these homologs has not been explored. Here, we use ATAC-seq, genome-wide histone modification mapping, and expression analysis to examine colorectal cancer cells lacking one or both ARID proteins. We find that ARID1A has a dominant role in maintaining chromatin accessibility at enhancers, while the contribution of ARID1B is evident only in the context of ARID1A mutation...
October 2, 2017: ELife
https://www.readbyqxmd.com/read/28951459/smyd5-controls-heterochromatin-and-chromosome-integrity-during-embryonic-stem-cell-differentiation
#16
Benjamin L Kidder, Runsheng He, Darawalee Wangsa, Hesed M Padilla-Nash, M Margarida Bernardo, Shijie Sheng, Thomas Ried, Keji Zhao
Epigenetic regulation of chromatin states is thought to control gene expression programs during lineage specification. However, the roles of repressive histone modifications such as trimethylated histone lysine 20 (H4K20me3) in development and genome stability are largely unknown. Here we show that depletion of SET and MYND domain-containing protein 5 (SMYD5), which mediates H4K20me3, leads to genome-wide decreases in H4K20me3 and H3K9me3 levels and derepression of endogenous LTR and LINE repetitive DNA elements during differentiation of mouse embryonic stem (ES) cells...
September 26, 2017: Cancer Research
https://www.readbyqxmd.com/read/28949456/dysregulation-of-histone-methyltransferases-in-breast-cancer-opportunities-for-new-targeted-therapies
#17
REVIEW
(no author information available yet)
Histone methyltransferases (HMTs) catalyze the methylation of lysine and arginine residues on histone tails and non-histone targets. These important post-translational modifications are exquisitely regulated and affect chromatin compaction and transcriptional programs leading to diverse biological outcomes. There is accumulating evidence that genetic alterations of several HMTs impinge on oncogenic or tumor-suppressor functions and influence both cancer initiation and progression. HMTs therefore represent an opportunity for therapeutic targeting in those patients with tumors in which HMTs are dysregulated, to reverse the histone marks and transcriptional programs associated with aggressive tumor behavior...
December 2016: Molecular Oncology
https://www.readbyqxmd.com/read/28937961/regulation-of-chromatin-assembly-and-cell-transformation-by-formaldehyde-exposure-in-human-cells
#18
Danqi Chen, Lei Fang, Shenglin Mei, Hongjie Li, Xia Xu, Thomas L Des Marais, Kun Lu, X Shirley Liu, Chunyuan Jin
BACKGROUND: Formaldehyde (FA) is an environmental and occupational chemical carcinogen. Recent studies have shown that exogenous FA causes only a modest increase in DNA adduct formation compared with the amount of adducts formed by endogenous FA, raising the possibility that epigenetic mechanisms may contribute to FA-mediated carcinogenicity. OBJECTIVES: We investigated the effects of FA exposure on histone modifications and chromatin assembly. We also examined the role of defective chromatin assembly in FA-mediated transcription and cell transformation...
September 21, 2017: Environmental Health Perspectives
https://www.readbyqxmd.com/read/28932035/epigenetics-in-oral-squamous-cell-carcinoma
#19
REVIEW
K N Hema, T Smitha, H S Sheethal, S Angeline Mirnalini
Oral squamous cell carcinoma (OSCC) is the most common type of oral neoplasm, accounting for over 90% of all oral malignancies and 38% of head and neck tumors. Worldwide, OSCC is the eighth most common human cancer, with more than 500,000 new cases being diagnosed every year with a fairly onerous prognosis, encouraging further research on factors that might modify disease outcome. Genetic and/or environmental risk factors associated with the development of oral cancer have been sufficiently understood (smoking, alcohol, betel, diet, living habits, etc...
May 2017: Journal of Oral and Maxillofacial Pathology: JOMFP
https://www.readbyqxmd.com/read/28930539/transcriptional-regulation-of-p57-kip2-expression-during-development-differentiation-and-disease
#20
Marianna N Rossi, Oriella Andresini, Francesca Matteini, Rossella Maione
p57(kip2) is the most complex member of the CIP/KIP family of cyclin-dependent kinase inhibitors and plays a fundamental role in regulating cell cycle and differentiation during mammalian development. Consistently with a key role for p57(kip2) in the spatial and temporal control of cell proliferation, its expression is fine-tuned by multiple regulatory mechanisms, resulting in a tissue-, developmental phase- and cell type-specific pattern. Moreover, p57(kip2) is an imprinted gene, further supporting the importance of its proper expression dosage...
January 1, 2018: Frontiers in Bioscience (Landmark Edition)
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