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Cell Cycle and Regulation
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Cell Cycle and Regulation

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (31 January 2019) | Viewed by 44083

Special Issue Editor

Dr. Ana María Zubiaga

E-Mail Website
Guest Editor
Molecular Biology of Cancer, University of the Basque Country, UPV/EHU, Leioa, Spain
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The process of cell division is critical to the growth and development of an organism. As a fertilized egg develops into a mature organism, tissues undergo cellular renewal or commit to terminal differentiation and leave the cell cycle. Tight regulation of events controlling the cell cycle ensures the integrity of the genetic information and prevents aberrant or unscheduled cell division. Dysregulation of this process can lead to various diseases, including cancer, autoimmunity or degenerative disorders.

Many molecular mechanisms control the cell cycle, and some of these take place in parallel and exhibit redundancy. A major level of control is carried out through the regulation of gene transcription. Entry and progression through, as well as exit from, the cell cycle require a series of well-coordinated transcriptional and epigenetic pathways to regulate the timely expression of hundreds of genes. Recent studies have been very helpful in identifying diverse transcriptional networks in the cell cycle. However, we are still far from full understanding of the transcriptional events operating in processes linked to the cell division cycle.

This Special Issue is focused on studies related to the genetic and epigenetic regulation of the cell cycle, from the analysis of cell cycle entry at quiescence and onward through to the study of cell cycle exit and terminal differentiation, and how this regulation is altered in stressful or pathological conditions, such as cancer.

We cordially invite researchers working actively in these fields to submit their original research or review manuscripts to this Special Issue on cell cycle regulation.

Dr. Ana María Zubiaga
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Genes is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Cell cycle
  • Gene expression
  • Gene regulation
  • Transcription profiling
  • Transcription factors
  • Chromatin remodeling and epigenetics
  • Cell-cycle progression
  • Cellular quiescence
  • Cell-cycle exit
  • Cellular differentiation
  • Cellular transformation
  • Cancer

Published Papers (8 papers)

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Editorial

Jump to: Research, Review

3 pages, 182 KiB  
Editorial
Foreword Special Issue Cell Cycle and Regulation
by Ana María Zubiaga
Genes 2020, 11(3), 254; https://0-doi-org.brum.beds.ac.uk/10.3390/genes11030254 - 27 Feb 2020
Cited by 2 | Viewed by 1906
Abstract
The process of cell division is critical to the growth and development of an organism [...] Full article
(This article belongs to the Special Issue Cell Cycle and Regulation)

Research

Jump to: Editorial, Review

12 pages, 2866 KiB  
Article
Anti-Colorectal Cancer Effects of Probiotic-Derived p8 Protein
by Byung Chull An, Sunwoong Hong, Ho Jin Park, Bong-Kyu Kim, Jun Young Ahn, Yongku Ryu, Jae Hyung An and Myung Jun Chung
Genes 2019, 10(8), 624; https://0-doi-org.brum.beds.ac.uk/10.3390/genes10080624 - 19 Aug 2019
Cited by 28 | Viewed by 4400
Abstract
Recently, we reported a novel therapeutic probiotic-derived protein, p8, which has anti-colorectal cancer (anti-CRC) properties. In vitro experiments using a CRC cell line (DLD-1), anti-proliferation activity (about 20%) did not improve after increasing the dose of recombinant-p8 (r-p8) to >10 μM. Here, we [...] Read more.
Recently, we reported a novel therapeutic probiotic-derived protein, p8, which has anti-colorectal cancer (anti-CRC) properties. In vitro experiments using a CRC cell line (DLD-1), anti-proliferation activity (about 20%) did not improve after increasing the dose of recombinant-p8 (r-p8) to >10 μM. Here, we show that this was due to the low penetrative efficiency of r-p8 exogenous treatment. Furthermore, we found that r-p8 entered the cytosol through endocytosis, which might be a reason for the low penetration efficiency. Therefore, to improve the therapeutic efficacy of p8, we tried to improve delivery to CRC cells. This resulted in endogenous expression of p8 and increased the anti-proliferative effects by up to 2-fold compared with the exogenous treatment (40 μM). Anti-migration activity also increased markedly. Furthermore, we found that the anti-proliferation activity of p8 was mediated by inhibition of the p53-p21-Cyclin B1/Cdk1 signal pathway, resulting in growth arrest at the G2 phase of the cell cycle. Taken together, these results suggest that p8 is toxic to cancer cells, shows stable expression within cells, and shows strong cancer suppressive activity by inducing cell cycle arrest. Therefore, p8 is a strong candidate for gene therapy if it can be loaded onto cancer-specific viruses. Full article
(This article belongs to the Special Issue Cell Cycle and Regulation)
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14 pages, 8819 KiB  
Article
Ankrd45 Is a Novel Ankyrin Repeat Protein Required for Cell Proliferation
by Yunsi Kang, Haibo Xie and Chengtian Zhao
Genes 2019, 10(6), 462; https://0-doi-org.brum.beds.ac.uk/10.3390/genes10060462 - 16 Jun 2019
Cited by 8 | Viewed by 3396
Abstract
Ankyrin repeats, the most common protein–protein interaction motifs in nature, are widely present in proteins of both eukaryotic and prokaryotic cells. Ankyrin repeat-containing proteins play diverse biological functions. Here, we identified the gene ankrd45, which encodes a novel, two ankyrin repeat-containing protein. Zebrafish [...] Read more.
Ankyrin repeats, the most common protein–protein interaction motifs in nature, are widely present in proteins of both eukaryotic and prokaryotic cells. Ankyrin repeat-containing proteins play diverse biological functions. Here, we identified the gene ankrd45, which encodes a novel, two ankyrin repeat-containing protein. Zebrafish ankrd45 displayed a tissue specific expression pattern during early development, with high expression in ciliated tissues, including otic vesicles, Kupffer’s vesicles, pronephric ducts, and floor plates. Surprisingly, zebrafish ankrd45 mutants were viable and developed grossly normal cilia. In contrast, mutant larvae developed enlarged livers when induced with liver specific expression of KrasG12V, one of the common mutations of KRAS that leads to cancer in humans. Further, histological analysis suggested that multiple cysts developed in the mutant liver due to cell apoptosis. Similarly, knockdown of ANKRD45 expression with either siRNA or CRISPR/Cas9 methods induced apoptosis in cultured cells, similar to those in zebrafish ankrd45 mutant livers after induction. Using different cell lines, we show that the distribution of ANKRD45 protein was highly dynamic during mitosis. ANKRD45 is preferably localized to the midbody ring during cytokinesis. Together, our results suggest that ANKRD45 is a novel ankyrin repeat protein with a conserved role during cell proliferation in both zebrafish embryos and mammalian cells. Full article
(This article belongs to the Special Issue Cell Cycle and Regulation)
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15 pages, 1984 KiB  
Article
Golgi Oncoprotein GOLPH3 Gene Expression Is Regulated by Functional E2F and CREB/ATF Promoter Elements
by Beatriz Peñalver-González, Jon Vallejo-Rodríguez, Gartze Mentxaka, Asier Fullaondo, Ainhoa Iglesias-Ara, Seth J. Field and Ana M. Zubiaga
Genes 2019, 10(3), 247; https://0-doi-org.brum.beds.ac.uk/10.3390/genes10030247 - 25 Mar 2019
Cited by 7 | Viewed by 3774
Abstract
The Golgi organelle duplicates its protein and lipid content to segregate evenly between two daughter cells after mitosis. However, how Golgi biogenesis is regulated during interphase remains largely unknown. Here we show that messenger RNA (mRNA) expression of GOLPH3 and GOLGA2, two [...] Read more.
The Golgi organelle duplicates its protein and lipid content to segregate evenly between two daughter cells after mitosis. However, how Golgi biogenesis is regulated during interphase remains largely unknown. Here we show that messenger RNA (mRNA) expression of GOLPH3 and GOLGA2, two genes encoding Golgi proteins, is induced specifically in G1 phase, suggesting a link between cell cycle regulation and Golgi growth. We have examined the role of E2F transcription factors, critical regulators of G1 to S progression of the cell cycle, in the expression of Golgi proteins during interphase. We show that promoter activity for GOLPH3, a Golgi protein that is also oncogenic, is induced by E2F1-3 and repressed by E2F7. Mutation of the E2F motifs present in the GOLPH3 promoter region abrogates E2F1-mediated induction of a GOLPH3 luciferase reporter construct. Furthermore, we identify a critical CREB/ATF element in the GOLPH3 promoter that is required for its steady state and ATF2-induced expression. Interestingly, depletion of GOLPH3 with small interfering RNA (siRNA) delays the G1 to S transition in synchronized U2OS cells. Taken together, our results reveal a link between cell cycle regulation and Golgi function, and suggest that E2F-mediated regulation of Golgi genes is required for the timely progression of the cell cycle. Full article
(This article belongs to the Special Issue Cell Cycle and Regulation)
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21 pages, 4942 KiB  
Article
Survivin Splice Variants in Arsenic Trioxide (As2O3)-Induced Deactivation of PI3K and MAPK Cell Signalling Pathways in MCF-7 Cells
by Kagiso Laka, Lilian Makgoo and Zukile Mbita
Genes 2019, 10(1), 41; https://0-doi-org.brum.beds.ac.uk/10.3390/genes10010041 - 14 Jan 2019
Cited by 17 | Viewed by 3456
Abstract
Several pathways are deregulated during carcinogenesis but most notably, tumour cells can lose cell cycle control and acquire resistance to apoptosis by expressing a number of anti-apoptotic proteins such as the Inhibitors of Apoptosis Protein (IAP) family of proteins that include survivin, which [...] Read more.
Several pathways are deregulated during carcinogenesis but most notably, tumour cells can lose cell cycle control and acquire resistance to apoptosis by expressing a number of anti-apoptotic proteins such as the Inhibitors of Apoptosis Protein (IAP) family of proteins that include survivin, which is implicated in cancer development. There is no study which had proven that arsenic trioxide (As2O3) has any effect on the splicing machinery of survivin and its splice variants, hence this study was aimed at determining the cytotoxic effect of As2O3 and its effect on the expression pattern of survivin splice variants in MCF-7 cells. As2O3 inhibited the growth of the MCF-7 cells in a concentration-dependent manner. The Muse® Cell Analyser showed that As2O3-induced G2/M cell cycle arrest, promoted caspase-dependent apoptosis without causing any damage to the mitochondrial membrane of MCF-7 cells. As2O3 also deactivated two survival pathways, Mitogen-Activated Protein Kinase (MAPK) and Phosphoinositide 3-Kinase (PI3K) signalling pathways in MCF-7 cells. Deactivation of the two pathways was accompanied by the upregulation of survivin 3α during As2O3-induced G2/M cell cycle arrest and apoptosis. Survivin 2B was found to be upregulated only during As2O3-induced G2/M cell cycle arrest but downregulated during As2O3-induced apoptosis. Survivin wild-type was highly expressed in the untreated MCF-7 cells, the expression was upregulated during As2O3-induced G2/M cell cycle arrest and it was downregulated during As2O3-induced apoptosis. Survivin variant ΔEx3 was undetected in both untreated and treated MCF-7 cells. Survivin proteins were localised in both the nucleus and cytoplasm in MCF-7 cells and highly upregulated during the As2O3-induced G2/M cell cycle arrest, which can be attributed to the upregulation of survivin-2B. This study has provided the first evidence showing that the novel survivin 2B splice variant may be involved in the regulation of As2O3-induced G2/M cell cycle arrest only. This splice variant can therefore, be targeted for therapeutic purposes against Luminal A breast cancer cells. Full article
(This article belongs to the Special Issue Cell Cycle and Regulation)
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Graphical abstract

16 pages, 2425 KiB  
Article
Oxidative Stress Causes Enhanced Secretion of YB-1 Protein that Restrains Proliferation of Receiving Cells
by Andrea Maria Guarino, Annaelena Troiano, Elio Pizzo, Andrea Bosso, Maria Vivo, Gabriella Pinto, Angela Amoresano, Alessandra Pollice, Girolama La Mantia and Viola Calabrò
Genes 2018, 9(10), 513; https://0-doi-org.brum.beds.ac.uk/10.3390/genes9100513 - 22 Oct 2018
Cited by 32 | Viewed by 5121
Abstract
The prototype cold-shock Y-box binding protein 1 (YB-1) is a multifunctional protein that regulates a variety of fundamental biological processes including cell proliferation and migration, DNA damage, matrix protein synthesis and chemotaxis. The plethora of functions assigned to YB-1 is strictly dependent on [...] Read more.
The prototype cold-shock Y-box binding protein 1 (YB-1) is a multifunctional protein that regulates a variety of fundamental biological processes including cell proliferation and migration, DNA damage, matrix protein synthesis and chemotaxis. The plethora of functions assigned to YB-1 is strictly dependent on its subcellular localization. In resting cells, YB-1 localizes to cytoplasm where it is a component of messenger ribonucleoprotein particles. Under stress conditions, YB-1 contributes to the formation of stress granules (SGs), cytoplasmic foci where untranslated messenger RNAs (mRNAs) are sorted or processed for reinitiation, degradation, or packaging into ribonucleoprotein particles (mRNPs). Following DNA damage, YB-1 translocates to the nucleus and participates in DNA repair thereby enhancing cell survival. Recent data show that YB-1 can also be secreted and YB-1-derived polypeptides are found in plasma of patients with sepsis and malignancies. Here we show that in response to oxidative insults, YB-1 assembly in SGs is associated with an enhancement of YB-1 protein secretion. An enriched fraction of extracellular YB-1 (exYB-1) significantly inhibited proliferation of receiving cells and such inhibition was associated to a G2/M cell cycle arrest, induction of p21WAF and reduction of ΔNp63α protein level. All together, these data show that acute oxidative stress causes sustained release of YB-1 as a paracrine/autocrine signal that stimulate cell cycle arrest. Full article
(This article belongs to the Special Issue Cell Cycle and Regulation)
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Review

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29 pages, 1675 KiB  
Review
MYC Oncogene Contributions to Release of Cell Cycle Brakes
by Lucía García-Gutiérrez, María Dolores Delgado and Javier León
Genes 2019, 10(3), 244; https://0-doi-org.brum.beds.ac.uk/10.3390/genes10030244 - 22 Mar 2019
Cited by 129 | Viewed by 13876
Abstract
Promotion of the cell cycle is a major oncogenic mechanism of the oncogene c-MYC (MYC). MYC promotes the cell cycle by not only activating or inducing cyclins and CDKs but also through the downregulation or the impairment of the activity of a set [...] Read more.
Promotion of the cell cycle is a major oncogenic mechanism of the oncogene c-MYC (MYC). MYC promotes the cell cycle by not only activating or inducing cyclins and CDKs but also through the downregulation or the impairment of the activity of a set of proteins that act as cell-cycle brakes. This review is focused on the role of MYC as a cell-cycle brake releaser i.e., how MYC stimulates the cell cycle mainly through the functional inactivation of cell cycle inhibitors. MYC antagonizes the activities and/or the expression levels of p15, ARF, p21, and p27. The mechanism involved differs for each protein. p15 (encoded by CDKN2B) and p21 (CDKN1A) are repressed by MYC at the transcriptional level. In contrast, MYC activates ARF, which contributes to the apoptosis induced by high MYC levels. At least in some cells types, MYC inhibits the transcription of the p27 gene (CDKN1B) but also enhances p27’s degradation through the upregulation of components of ubiquitin ligases complexes. The effect of MYC on cell-cycle brakes also opens the possibility of antitumoral therapies based on synthetic lethal interactions involving MYC and CDKs, for which a series of inhibitors are being developed and tested in clinical trials. Full article
(This article belongs to the Special Issue Cell Cycle and Regulation)
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14 pages, 5500 KiB  
Review
The Mitotic Cancer Target Polo-Like Kinase 1: Oncogene or Tumor Suppressor?
by Guillermo de Cárcer
Genes 2019, 10(3), 208; https://0-doi-org.brum.beds.ac.uk/10.3390/genes10030208 - 11 Mar 2019
Cited by 50 | Viewed by 7099
Abstract
The master mitotic regulator, Polo-like kinase 1 (Plk1), is an essential gene for the correct execution of cell division. Plk1 has strong clinical relevance, as it is considered a bona fide cancer target, it is found overexpressed in a large collection of different [...] Read more.
The master mitotic regulator, Polo-like kinase 1 (Plk1), is an essential gene for the correct execution of cell division. Plk1 has strong clinical relevance, as it is considered a bona fide cancer target, it is found overexpressed in a large collection of different cancer types and this tumoral overexpression often correlates with poor patient prognosis. All these data led the scientific community to historically consider Plk1 as an oncogene. Although there is a collection of scientific reports showing how Plk1 can contribute to tumor progression, recent data from different laboratories using mouse models, show that Plk1 can surprisingly play as a tumor suppressor. Therefore, the fact that Plk1 is an oncogene is now under debate. This review summarizes the proposed mechanisms by which Plk1 can play as an oncogene or as a tumor suppressor, and extrapolates this information to clinical features. Full article
(This article belongs to the Special Issue Cell Cycle and Regulation)
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