scholarly journals Oxyresveratrol Modulates Gene Expression of Apoptosis, Cell Cycle Control and DNA Repair in MCF7 Cells

2021 ◽  
Vol 12 ◽  
Author(s):  
Sarayut Radapong ◽  
Kelvin Chan ◽  
Satyajit D. Sarker ◽  
Kenneth J. Ritchie
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Dna Repair ◽  
Biological Activities ◽  
Chromatin Condensation ◽  
Cell Cycle Control ◽  
Expression Patterns ◽  
Treated Group ◽  
Pcr Analysis ◽  
Mcf7 Cells

Oxyresveratrol (OXY) is a small molecule of phytochemical known as hydroxystilbenoids, which have been reported significantly important biological activities. The aim of this study was to elucidate the gene expression and biological pathways altered in MCF7, breast cancer cells. The cytotoxicity to different cancer cell lines was screened using MTT assay and then whole gene expression was elucidated using microarray. The pathways selected also validated by quantitative PCR analysis, fluorometric and western blot assay. A total of 686 genes were found to have altered mRNA expression levels of two-fold or more in the 50 μM OXY-treated group, while 2,338 genes were differentially expressed in the 100 µM-treated group. The relevant visualized global expression patterns of genes and pathways were generated. Apoptosis was activated through mitochondria-lost membrane potential, caspase-3 expression and chromatin condensation without DNA damage. G0/G1 and S phases of the cell cycle control were inhibited dose-dependently by the compound. Rad51 gene (DNA repair pathway) was significantly down-regulated (p < 0.0001). These results indicated that OXY moderated the key genes and pathways in MCF7 cells that could be developed as chemotherapy or chemo-sensitizing agent.

scholarly journals The Gene Targeting Approach of Small Fragment Homologous Replacement (SFHR) Alters the Expression Patterns of DNA Repair and Cell Cycle Control Genes

2016 ◽  
Vol 5 ◽  
pp. e304 ◽  
Author(s):  
Silvia Pierandrei ◽  
Andrea Luchetti ◽  
Massimo Sanchez ◽  
Giuseppe Novelli ◽  
Federica Sangiuolo ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Repair ◽  
Gene Targeting ◽  
Cell Cycle Control ◽  
Expression Patterns ◽  
Small Fragment

scholarly journals Symbiosis maintenance in the facultative coral, Oculina arbuscula, relies on nitrogen cycling, cell cycle modulation, and immunity

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
H. E. Rivera ◽  
S. W. Davies
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Nitrogen Cycling ◽  
Physiological Stress ◽  
Cell Cycle Control ◽  
Expression Patterns ◽  
Cycling Cell ◽  
Unicellular Algae ◽  
Oculina Arbuscula ◽  
Baseline Conditions

AbstractSymbiosis with unicellular algae in the family Symbiodiniaceae is common across tropical marine invertebrates. Reef-building corals offer a clear example of cellular dysfunction leading to a dysbiosis that disrupts entire ecosystems in a process termed coral bleaching. Due to their obligate symbiotic relationship, understanding the molecular underpinnings that sustain this symbiosis in tropical reef-building corals is challenging, as any aposymbiotic state is inherently coupled with severe physiological stress. Here, we leverage the subtropical, facultatively symbiotic and calcifying coral Oculina arbuscula to investigate gene expression differences between aposymbiotic and symbiotic branches within the same colonies under baseline conditions. We further compare gene ontology (GO) and KOG enrichment in gene expression patterns from O. arbuscula with prior work in the sea anemone Exaiptasia pallida (Aiptasia) and the salamander Ambystoma maculatum—both of which exhibit endophotosymbiosis with unicellular algae. We identify nitrogen cycling, cell cycle control, and immune responses as key pathways involved in the maintenance of symbiosis under baseline conditions. Understanding the mechanisms that sustain a healthy symbiosis between corals and Symbiodiniaceae algae is of urgent importance given the vulnerability of these partnerships to changing environmental conditions and their role in the continued functioning of critical and highly diverse marine ecosystems.

scholarly journals Interactions of CCAAT/enhancer-binding protein β with transcriptional coregulators

2016 ◽  
Vol 62 (3) ◽  
pp. 343-348
Author(s):  
Maria Miller
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Biological Activities ◽  
Cell Cycle Control ◽  
Specific Gene ◽  
Sequence Motifs ◽  
Protein Partners ◽  
Enhancer Binding Protein ◽  
Transcriptional Coregulators ◽  
Dna Sequence Motifs

CCAAT/enhancer-binding proteins (C/EBPs) are key regulators of numerous cellular pro-cesses, including cell proliferation, differentiation, and tumorigenesis. Their biological activities require interactions with several protein partners and the formation of functional multiprotein complexes involved in DNA repair and cell cycle control. Members of the fam-ily (C/EBPα, β, δ, ε, and γ) bind to common DNA sequence motifs as homo- or hetero-dimers and interact with other transcription factors to control transcription of a number of eukary-otic genes. Of particular interest is C/EBPβ, which binds to closed chromatin and acts as a pioneering factor for initiating tissue-specific gene expression at several promoters. This review focuses on intermolecular interactions that underlie C/EBPβ’s ability to regulate chro-matin accessibility and directs readers to general reviews describing transcription regulation in eukaryotes.

983: Bladder Cancer Predisposition: A Pathway-Based Approach to DNA Repair and Cell Cycle Control Genes

2006 ◽  
Vol 175 (4S) ◽  
pp. 317-317
Author(s):  
Xifeng Wu ◽  
Jian Gu ◽  
H. Barton Grossman ◽  
Christopher I. Amos ◽  
Carol Etzel ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bladder Cancer ◽  
Dna Repair ◽  
Cell Cycle Control ◽  
Cancer Predisposition

scholarly journals Arsenic hexoxide has differential effects on cell proliferation and genome-wide gene expression in human primary mammary epithelial and MCF7 cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Donguk Kim ◽  
Na Yeon Park ◽  
Keunsoo Kang ◽  
Stuart K. Calderwood ◽  
Dong-Hyung Cho ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Mammary Epithelial ◽  
Mcf7 Cells ◽  
Differential Effects ◽  
Cycle Arrest ◽  
Genome Wide ◽  
Human Mammary Epithelial ◽  
Genome Wide Gene Expression

AbstractArsenic is reportedly a biphasic inorganic compound for its toxicity and anticancer effects in humans. Recent studies have shown that certain arsenic compounds including arsenic hexoxide (AS4O6; hereafter, AS6) induce programmed cell death and cell cycle arrest in human cancer cells and murine cancer models. However, the mechanisms by which AS6 suppresses cancer cells are incompletely understood. In this study, we report the mechanisms of AS6 through transcriptome analyses. In particular, the cytotoxicity and global gene expression regulation by AS6 were compared in human normal and cancer breast epithelial cells. Using RNA-sequencing and bioinformatics analyses, differentially expressed genes in significantly affected biological pathways in these cell types were validated by real-time quantitative polymerase chain reaction and immunoblotting assays. Our data show markedly differential effects of AS6 on cytotoxicity and gene expression in human mammary epithelial normal cells (HUMEC) and Michigan Cancer Foundation 7 (MCF7), a human mammary epithelial cancer cell line. AS6 selectively arrests cell growth and induces cell death in MCF7 cells without affecting the growth of HUMEC in a dose-dependent manner. AS6 alters the transcription of a large number of genes in MCF7 cells, but much fewer genes in HUMEC. Importantly, we found that the cell proliferation, cell cycle, and DNA repair pathways are significantly suppressed whereas cellular stress response and apoptotic pathways increase in AS6-treated MCF7 cells. Together, we provide the first evidence of differential effects of AS6 on normal and cancerous breast epithelial cells, suggesting that AS6 at moderate concentrations induces cell cycle arrest and apoptosis through modulating genome-wide gene expression, leading to compromised DNA repair and increased genome instability selectively in human breast cancer cells.

scholarly journals Histone modifications form a cell-type-specific chromosomal bar code that persists through the cell cycle

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
John A. Halsall ◽  
Simon Andrews ◽  
Felix Krueger ◽  
Charlotte E. Rutledge ◽  
Gabriella Ficz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Histone Modifications ◽  
Expression Patterns ◽  
Cell Types ◽  
Cell Type ◽  
Bar Code ◽  
Genes Encoding ◽  
Cell Type Specific ◽  
Rolling Windows

AbstractChromatin configuration influences gene expression in eukaryotes at multiple levels, from individual nucleosomes to chromatin domains several Mb long. Post-translational modifications (PTM) of core histones seem to be involved in chromatin structural transitions, but how remains unclear. To explore this, we used ChIP-seq and two cell types, HeLa and lymphoblastoid (LCL), to define how changes in chromatin packaging through the cell cycle influence the distributions of three transcription-associated histone modifications, H3K9ac, H3K4me3 and H3K27me3. We show that chromosome regions (bands) of 10–50 Mb, detectable by immunofluorescence microscopy of metaphase (M) chromosomes, are also present in G1 and G2. They comprise 1–5 Mb sub-bands that differ between HeLa and LCL but remain consistent through the cell cycle. The same sub-bands are defined by H3K9ac and H3K4me3, while H3K27me3 spreads more widely. We found little change between cell cycle phases, whether compared by 5 Kb rolling windows or when analysis was restricted to functional elements such as transcription start sites and topologically associating domains. Only a small number of genes showed cell-cycle related changes: at genes encoding proteins involved in mitosis, H3K9 became highly acetylated in G2M, possibly because of ongoing transcription. In conclusion, modified histone isoforms H3K9ac, H3K4me3 and H3K27me3 exhibit a characteristic genomic distribution at resolutions of 1 Mb and below that differs between HeLa and lymphoblastoid cells but remains remarkably consistent through the cell cycle. We suggest that this cell-type-specific chromosomal bar-code is part of a homeostatic mechanism by which cells retain their characteristic gene expression patterns, and hence their identity, through multiple mitoses.

scholarly journals Mutational analyses of fs(1)Ya, an essential, developmentally regulated, nuclear envelope protein in Drosophila.

Genetics ◽  
1995 ◽  
Vol 141 (4) ◽  
pp. 1473-1481 ◽  
Author(s):  
J Liu ◽  
K Song ◽  
M F Wolfner
Keyword(s):  
Cell Cycle ◽  
Embryonic Development ◽  
Nuclear Envelope ◽  
Envelope Protein ◽  
Chromatin Condensation ◽  
Cell Cycle Control ◽  
Nuclear Lamina ◽  
Mitotic Division ◽  
Developmentally Regulated ◽  
Egg Maturation

Abstract The fs(1)Ya protein (YA) is an essential, maternally encoded, nuclear lamina protein that is under both developmental and cell cycle control. A strong Ya mutation results in early arrest of embryos. To define the function of YA in the nuclear envelope during early embryonic development, we characterized the phenotypes of four Ya mutants alleles and determined their molecular lesions. Ya mutant embryos arrest with abnormal nuclear envelopes prior to the first mitotic division; a proportion of embryos from two leaky Ya mutants proceed beyond this but arrest after several abnormal divisions. Ya unfertilized eggs contain nuclei of different sizes and condensation states, apparently due to abnormal fusion of the meiotic products immediately after meiosis. Lamin is localized at the periphery of the uncondensed nuclei in these eggs. These results suggest that YA function is required during and after egg maturation to facilitate proper chromatin condensation, rather than to allow a lamin-containing nuclear envelope to form. Two leaky Ya alleles that partially complement have lesions at opposite ends of the YA protein, suggesting that the N- and C-termini are important for YA function and that YA might interact with itself either directly or indirectly.

Cell cycle control of gene expression in yeast

1992 ◽  
Vol 2 (12) ◽  
pp. 353-357 ◽  
Author(s):  
Leland H. Johnston
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Cell Cycle Control ◽  
Control Of Gene Expression

Retinoblastoma Protein, Gene Expression, and Cell Cycle Control

Cancer Genes ◽  
1996 ◽  
pp. 177-191
Author(s):  
Jane Clifford Azizkhan ◽  
Shiaw Yih Lin ◽  
David Jensen ◽  
Dusan Kostic ◽  
Adrian R. Black
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Protein Gene ◽  
Cell Cycle Control ◽  
Retinoblastoma Protein
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