scholarly journals Alu RNA Modulates the Expression of Cell Cycle Genes in Human Fibroblasts

2019 ◽  
Vol 20 (13) ◽  
pp. 3315 ◽  
Author(s):  
Simona Cantarella ◽  
Davide Carnevali ◽  
Marco Morselli ◽  
Anastasia Conti ◽  
Matteo Pellegrini ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Human Fibroblasts ◽  
Rna Polymerase Iii ◽  
Protein Coding ◽  
Non Coding Rna ◽  
Genome Wide ◽  
Hela Cell Lines ◽  
Significant Enrichment ◽  
Alu Rna

Alu retroelements, whose retrotransposition requires prior transcription by RNA polymerase III to generate Alu RNAs, represent the most numerous non-coding RNA (ncRNA) gene family in the human genome. Alu transcription is generally kept to extremely low levels by tight epigenetic silencing, but it has been reported to increase under different types of cell perturbation, such as viral infection and cancer. Alu RNAs, being able to act as gene expression modulators, may be directly involved in the mechanisms determining cellular behavior in such perturbed states. To directly address the regulatory potential of Alu RNAs, we generated IMR90 fibroblasts and HeLa cell lines stably overexpressing two slightly different Alu RNAs, and analyzed genome-wide the expression changes of protein-coding genes through RNA-sequencing. Among the genes that were upregulated or downregulated in response to Alu overexpression in IMR90, but not in HeLa cells, we found a highly significant enrichment of pathways involved in cell cycle progression and mitotic entry. Accordingly, Alu overexpression was found to promote transition from G1 to S phase, as revealed by flow cytometry. Therefore, increased Alu RNA may contribute to sustained cell proliferation, which is an important factor of cancer development and progression.

scholarly journals Emerging Roles of Estrogen-Regulated Enhancer and Long Non-Coding RNAs

2020 ◽  
Vol 21 (10) ◽  
pp. 3711
Author(s):  
Melina J. Sedano ◽  
Alana L. Harrison ◽  
Mina Zilaie ◽  
Chandrima Das ◽  
Ramesh Choudhari ◽  
...  
Keyword(s):  
Rna Sequencing ◽  
Expression Patterns ◽  
Biological Significance ◽  
Rna Seq ◽  
Biological Functions ◽  
Protein Coding ◽  
Rna Molecules ◽  
Non Coding Rna ◽  
Genome Wide ◽  
Non Coding Rnas

Genome-wide RNA sequencing has shown that only a small fraction of the human genome is transcribed into protein-coding mRNAs. While once thought to be “junk” DNA, recent findings indicate that the rest of the genome encodes many types of non-coding RNA molecules with a myriad of functions still being determined. Among the non-coding RNAs, long non-coding RNAs (lncRNA) and enhancer RNAs (eRNA) are found to be most copious. While their exact biological functions and mechanisms of action are currently unknown, technologies such as next-generation RNA sequencing (RNA-seq) and global nuclear run-on sequencing (GRO-seq) have begun deciphering their expression patterns and biological significance. In addition to their identification, it has been shown that the expression of long non-coding RNAs and enhancer RNAs can vary due to spatial, temporal, developmental, or hormonal variations. In this review, we explore newly reported information on estrogen-regulated eRNAs and lncRNAs and their associated biological functions to help outline their markedly prominent roles in estrogen-dependent signaling.

GATA-2 Controls Proliferation of Megakaryocyte Progenitors and Its Expression Contributes to Human DS-AMKL.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 1380-1380
Author(s):  
Zan Huang ◽  
John Crispino
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Blast Crisis ◽  
Myelogenous Leukemia ◽  
Chromosome 21 ◽  
Cell Cycle Regulators ◽  
Megakaryoblastic Leukemia ◽  
Aberrant Gene Expression ◽  
Genome Wide ◽  
Aberrant Gene

Abstract GATA2 is an essential transcription factor that regulates multiple aspects of hematopoiesis. Mutations in GATA2 are associated with blast crisis phase of chronic myelogenous leukemia (CML) while overexpression of GATA2 is a hallmark of Down syndrome acute megakaryoblastic leukemia (DS-AMKL), a malignancy that is defined by the combination of trisomic chromosome 21 and a GATA1 mutation. Here, we show thatGATA2 is essential for megakaryocyte development from both wild-type and GATA-1mutant hematopoietic progenitors. Furthermore, we reveal that GATA2 is indispensable for cell cycle progression and that its expression cooperates with activated JAK3 to promote TPO-independent expansion of megakaryocytes. Genome-wide microarray analysis revealed that GATA2 regulates a wide set of genes including cell cycle regulators and lineage-specific genes that are essential for terminal differentiation of megakaryocytes. Of note, a subset of genes within the GATA2 signature is contained within human DS-AMKL patient specimens. These observations implicate overexpression of GATA2 in the aberrant gene expression and proliferation of AMKL. Taken together, our data demonstrate thatGATA2 is a critical regulator of normal and malignant megakaryopoiesis.

scholarly journals The long non-coding RNA LINC00152 is essential for cell cycle progression through mitosis in HeLa cells

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Linda Nötzold ◽  
Lukas Frank ◽  
Minakshi Gandhi ◽  
Maria Polycarpou-Schwarz ◽  
Matthias Groß ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Hela Cells ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals The Epstein-Barr Virus Immediate-Early Protein BZLF1 Induces Expression of E2F-1 and Other Proteins Involved in Cell Cycle Progression in Primary Keratinocytes and Gastric Carcinoma Cells

2002 ◽  
Vol 76 (24) ◽  
pp. 12543-12552 ◽  
Author(s):  
Amy Mauser ◽  
Elizabeth Holley-Guthrie ◽  
Adam Zanation ◽  
Wendall Yarborough ◽  
William Kaufmann ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Cyclin E ◽  
Human Fibroblasts ◽  
Cell Types ◽  
S Phase ◽  
Cycle Progression ◽  
Stem Loop ◽  
Barr Virus ◽  
Early Protein

ABSTRACT The Epstein-Barr virus (EBV) immediate-early protein BZLF1 mediates the switch between the latent and lytic forms of EBV infection and has been previously shown to induce a G1/S block in cell cycle progression in some cell types. To examine the effect of BZLF1 on cellular gene expression, we performed microarray analysis on telomerase-immortalized human keratinocytes that were mock infected or infected with a control adenovirus vector (AdLacZ) or a vector expressing the EBV BZLF1 protein (AdBZLF1). Cellular genes activated by BZLF1 expression included E2F-1, cyclin E, Cdc25A, and a number of other genes involved in cell cycle progression. Immunoblot analysis confirmed that BZLF1 induced expression of E2F-1, cyclin E, Cdc25A, and stem loop binding protein (a protein known to be primarily expressed during S phase) in telomerase-immortalized keratinocytes. Similarly, BZLF1 increased expression of E2F-1, cyclin E, and stem loop binding protein (SLBP) in primary tonsil keratinocytes. In contrast, BZLF1 did not induce E2F-1 expression in normal human fibroblasts. Cell cycle analysis revealed that while BZLF1 dramatically blocked G1/S progression in normal human fibroblasts, it did not significantly affect cell cycle progression in primary human tonsil keratinocytes. Furthermore, in EBV-infected gastric carcinoma cells, the BZLF1-positive cells had an increased number of cells in S phase compared to the BZLF1-negative cells. Thus, in certain cell types (but not others), BZLF1 enhances expression of cellular proteins associated with cell cycle progression, which suggests that an S-phase-like environment may be advantageous for efficient lytic EBV replication in some cell types.

scholarly journals Cytoskeletal integrity is required throughout the mitogen stimulation phase of the cell cycle and mediates the anchorage-dependent expression of cyclin D1.

1996 ◽  
Vol 7 (1) ◽  
pp. 101-111 ◽  
Author(s):  
R M Böhmer ◽  
E Scharf ◽  
R K Assoian
Keyword(s):  
Cell Cycle ◽  
Cell Adhesion ◽  
Cyclin D1 ◽  
Cell Cycle Progression ◽  
Human Fibroblasts ◽  
Cytochalasin D ◽  
Phase Cell ◽  
Dependent Part ◽  
Molecular Events ◽  
Normal Human

The proliferation of many nontransformed cells depends on cell adhesion. We report here that disrupting the cytoskeleton in normal human fibroblasts causes the same cell cycle phenotype that is observed after blocking cell adhesion: suspended cells and cytochalasin D-treated monolayers fail to progress through G1 despite normal mitogen-induced expression of c-myc mRNA. Midway between G0 and the beginning of S-phase, cell cycle progression becomes independent of adhesion and the cytoskeleton. At this stage, the cells are also mitogen independent. Molecular analyses showed that Rb hyperphosphorylation and the induction of cyclin D1 occur slightly earlier than the transition to cytoskeleton independence. Moreover, these molecular events are blocked by cytochalasin D. Overall, our data indicate the following: 1) anchorage and cytoskeletal integrity are required throughout the mitogen-dependent part of G1; 2) mitogens and the cytoskeleton jointly regulate the phosphorylation of Rb; and 3) this interdependence is manifest in the regulation of cyclin D1.

scholarly journals Cell cycle progression after cleavage failure

2004 ◽  
Vol 165 (5) ◽  
pp. 609-615 ◽  
Author(s):  
Yumi Uetake ◽  
Greenfield Sluder
Keyword(s):  
Cell Cycle ◽  
Cell Line ◽  
Mammalian Cells ◽  
Cell Cycle Progression ◽  
Human Fibroblasts ◽  
Human Cell Line ◽  
Cycle Progression ◽  
Binucleate Cells ◽  
Normal Human ◽  
Cleavage Failure

Failure of cells to cleave at the end of mitosis is dangerous to the organism because it immediately produces tetraploidy and centrosome amplification, which is thought to produce genetic imbalances. Using normal human and rat cells, we reexamined the basis for the attractive and increasingly accepted proposal that normal mammalian cells have a “tetraploidy checkpoint” that arrests binucleate cells in G1, thereby preventing their propagation. Using 10 μM cytochalasin to block cleavage, we confirm that most binucleate cells arrest in G1. However, when we use lower concentrations of cytochalasin, we find that binucleate cells undergo DNA synthesis and later proceed through mitosis in >80% of the cases for the hTERT-RPE1 human cell line, primary human fibroblasts, and the REF52 cell line. These observations provide a functional demonstration that the tetraploidy checkpoint does not exist in normal mammalian somatic cells.

scholarly journals An Evolving Role for the Long Non-Coding RNA H19 in Aging and Senescence

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 563-563
Author(s):  
Christian Sell ◽  
Manali Potnis
Keyword(s):  
Cell Cycle ◽  
Somatic Cell ◽  
Cell Fate ◽  
Cell Cycle Progression ◽  
Adult Stem Cells ◽  
Somatic Cells ◽  
Gene Transcript ◽  
Cell Fate Decisions ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract The long non-coding RNA (lncRNA) H19 is a maternally imprinted gene transcript that, in conjunction with the neighboring Igf2 gene, is critical in controlling embryonic growth. Loss of H19 results in fetal overgrowth associated with Beckwith Weidemann syndrome, while elevated H19 occurs in human cancers. In the adult, H19 functions in cancer cells where it promotes migration and is correlated with poor prognosis, and in adult stem cells where it is a key regulator of cell fate decisions during differentiation. While the function of H19 in primary somatic cells has not been defined, a reduction in the abundance of H19 has been reported during senescence in endothelial cells. Given the critical importance of H19 in cell fate decisions, it is likely that understanding the precise function of H19 in somatic cells in general and why reduced levels occur with cellular senescence will provide novel insights into both somatic cell maintenance and the senescence program. Towards this end, we examined the role of H19 in somatic cell growth using cardiac interstitial fibroblasts. Our results indicate that H19 is not only vital for somatic cell proliferation and survival, but that depletion of H19 leads to cell cycle arrest and the formation of abnormal nuclei resulting in senescent cells. We are defining both the upstream regulators of H19 and the downstream mediators of senescence following H19 depletion. Overall, these results indicate an essential role for H19 in cell cycle progression, chromatin structure, and possibly proper mitotic division.

scholarly journals Genome-Wide Identification and Analysis of Cell Cycle Genes in Betula pendula

2021 ◽  
Author(s):  
Yijie Li ◽  
Song Chen ◽  
Yuhang Liu ◽  
Haijiao Huang
Keyword(s):  
Cell Cycle ◽  
Growth And Development ◽  
Betula Pendula ◽  
Cell Cycle Progression ◽  
Transcript Abundance ◽  
Specific Expression ◽  
Cell Cycles ◽  
Cell Cycle Genes ◽  
Functional Studies ◽  
Genome Wide

Research Highlights: This study identified the cell cycle genes in birch that likely play important roles during plant growth and development. This provides a basis for understanding the regulatory mechanism of various cell cycles in Betula pendula. Background and Objectives: The cell cycle factors not only influence cell cycle progression together, but also regulate accretion, division and differentiation of cells, and then regulate growth and development of plant. In this study, we identified the putative cell cycle genes in B. pendula genome, based on the annotated cell cycle genes in A. thaliana. It could serve as a foundation for further functional studies. Materials and Methods: The transcript abundance was determined for all the cell cycle genes in xylem, root, leaf and flower tissues using RNA-seq technology. Results: We identified 59cell cycle gene models in the genome of B. pendula, 17 highly expression genes among them. These genes were BpCDKA.1, BpCDKB1.1, BpCDKB2.1, BpCKS1.2, BpCYCB1.1, BpCYCB1.2, BpCYCB2.1, BpCYCD3.1, BpCYCD3.5, BpDEL1, BpDpa2, BpE2Fa, BpE2Fb, BpKRP1, BpKRP2, BpRb1 and BpWEE1. Conclusions: We identified 17 core cell cycle genes in the genome of birch by combining phylogenetic analysis and tissue specific expression data.

scholarly journals Human Cytomegalovirus UL69 Protein Induces Cells To Accumulate in G1 Phase of the Cell Cycle

1999 ◽  
Vol 73 (1) ◽  
pp. 676-683 ◽  
Author(s):  
Mansuo Lu ◽  
Thomas Shenk
Keyword(s):  
Cell Cycle ◽  
Human Cytomegalovirus ◽  
Cell Cycle Progression ◽  
Human Fibroblasts ◽  
Protein A ◽  
S Phase ◽  
Cycle Progression ◽  
Multiple Points ◽  
Cell Cycle Block ◽  
Arrest Cell Cycle Progression

ABSTRACT Earlier studies have revealed that human cytomegalovirus rapidly inhibits the growth of fibroblasts, blocking cell cycle progression at multiple points, including the G1-to-S-phase transition. The present study demonstrates that the UL69 protein, a virus-encoded constituent of the virion, is able to arrest cell cycle progression when introduced into uninfected cells. Expression of the UL69 protein causes U2 OS cells and primary human fibroblasts to accumulate within the G1 compartment of the cell cycle, and serum fails to induce the progression of quiescent human fibroblasts into the S phase when the protein is present. Therefore, the UL69 protein is at least partially responsible for the cell cycle block that is instituted after infection of permissive cells with human cytomegalovirus.

Sign in / Sign up

Export Citation Format

Share Document