Read e-book Cell Cycle Deregulation in Cancer (Current Cancer Research)

Free download. Book file PDF easily for everyone and every device. You can download and read online Cell Cycle Deregulation in Cancer (Current Cancer Research) file PDF Book only if you are registered here. And also you can download or read online all Book PDF file that related with Cell Cycle Deregulation in Cancer (Current Cancer Research) book. Happy reading Cell Cycle Deregulation in Cancer (Current Cancer Research) Bookeveryone. Download file Free Book PDF Cell Cycle Deregulation in Cancer (Current Cancer Research) at Complete PDF Library. This Book have some digital formats such us :paperbook, ebook, kindle, epub, fb2 and another formats. Here is The CompletePDF Book Library. It's free to register here to get Book file PDF Cell Cycle Deregulation in Cancer (Current Cancer Research) Pocket Guide.

  1. The Open Clinical Cancer Journal
  2. The therapeutic potential of cell cycle targeting in multiple myeloma
  3. The Hallmarks of Cancer - Wikipedia
  4. Bibliographic Information

Correlated with the loss of functional tumor suppressors, transcriptional deregulation of Plk1 is reported in various cancers and associated with CIN and oncogenic transformation In co-ordination with the loss-of-function of tumor suppressors, the overexpression of this protein is associated with CIN and cancer 77 — Oncoproteins like EWS-Fli1 and Myc upregulate expression of aurora family proteins through binding on promoter response elements. On the other hand, tumor suppressors like p53, Brd4 also influence expression of Aurora kinases 83 — In fact, the altered expression of Aurora kinases are potential markers of cancer progression Regulated expression of kinetochore protein Hec1 is directly related to phosphorylation-mediated inactivation of Rb during the course of cell cycle.

Beside this, the CREB family of oncoprotein transcription factors has been shown to upregulate the levels of kinetochore protein Hec1 Disrupted pRb function is associated with transcriptional upregulation of Hec1, which may cause aneuploidy and tumor formation 89 , The initial events of mitosis are followed by chromosomal alignment at the equatorial plane of the cell during metaphase.

The amphitelic metaphase alignment precedes SAC release, chromosomal segregation, and entry into anaphase. Different transcription factors and chromatin modifiers regulate cell cycle specific promoter activities of these genes 68 , 92 , Upon genotoxic stress, Cdc20 expression is indirectly suppressed by p53 through pdependent mechanism On the other hand, a direct p53 binding element has been identified on the CDC20 promoter and shown to bring about repression of transcription through chromatin remodeling Similarly, direct recruitment of p53 on the promoter consensus element brings about chromatin remodeling and the repression of Mad1 expression Expression of Mad2 is regulated by E2F in a cell cycle-dependent manner.

Rb inactivation leads to aberrant Mad2 expression by deregulating E2F activity and contributes to mitotic defects and aneuploidy Cancer-associated defects in these tumor suppressors contribute to the abnormal expression of these proteins and a flawed SAC. Indeed, transcriptional abnormalities including differential promoter methylation of these SAC proteins are potential markers of cancers of various origins 97 , Their deregulated expressions are associated with CIN phenotype and incidence of cancer 6. The final stages of mitosis involve cytokinesis and mitotic exit.

Along with mitotic kinases like Aurora, Polo, and related families, some other molecular components also regulate this stage of the cell cycle. Protein regulator of cytokinesis 1 PRC1 and the guanine nucleotide exchange factor, Ect2, the two major molecules of cytokinesis have been related with cancer-associated altered expressions and CIN 6. In conclusion, we have summarized a number of reports from the ever-growing lists of proto-onco gene as well as tumor suppressor trans-factors in regulation of mitosis and their deregulation in tumor background Table 1. Table 1. Role of proto-oncoprotein and tumor suppressor transcription factors in mitosis and involvement in oncogenesis.

The role of transcriptional regulatory pathways behind the incidence of tumorigenesis remains an enigma. For a number of key cell cycle regulators, the transcriptional control represents an evolutionarily conserved mechanism to precisely maintain their abundance, working in conjunction with miRNA mediated silencing, translational control, and ubiquitin-mediated degradation 23 , 26 , , Among these cell cycle regulators, a defined set of factors stringently control mitotic entry, progression, and exit.

The interplay among these factors is naturally adjusted by their abundance. Abnormality in this abundance is associated with the occurrence of aneuploidy, a hallmark of cancer 2 , 8 , In this review, we have discussed the maintenance of protein levels of the mitotic players whose transcription is regulated in a cell cycle specific manner. We further discussed the deregulation of their transcriptional control, working in concert with cancer onset. In this regard, mutations in various tumor suppressors and proto-oncogenes acting as co-factors of transcription are found to disharmonize the relative protein levels, rather than mutations in the mitotic genes themselves.

Besides this, a few mitotic genes are reported to participate in transcriptional control. Furthermore, the list of transcripts whose transcription is affected by certain cell cycle or developmental transitions is being expanded owing to new genome-wide approaches. Answer to many open questions regarding the interplay between transcriptional regulation and mitotic progression will make an important contribution to the understanding of cell cycle control.

This, in turn, will help to dissect the involvement of cell cycle progression in the onset of tumorigenesis. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Jallepalli PV, Lengauer C. Chromosome segregation and cancer: cutting xthrough the mystery. Nat Rev Cancer 1 — Aneuploidy and cancer.

  1. The Gods Among Us (Divine Masquerade Series Book 1).
  2. A Modern English Grammar on Historical Principles: Volume 3 (Otto Jespersen).
  3. Waiting for Ricky Tantrum.
  4. Bridge of Sighs.
  5. An Introduction to Waves and Oscillations in the Sun (Astronomy and Astrophysics Library).
  6. What Could Possibly Go Wrong?;
  7. Cell cycle checkpoint in cancer: a therapeutically targetable double-edged sword.

J Cell Biochem —8. Boveri revisited: chromosomal instability, aneuploidy and tumorigenesis.

Navigation menu

Nat Rev Mol Cell Biol 10 — Losing balance: the origin and impact of aneuploidy in cancer. EMBO Rep 13 — Pfau SJ, Amon A. Chromosomal instability and aneuploidy in cancer: from yeast to man. A census of mitotic cancer genes: new insights into tumor cell biology and cancer therapy. Carcinogenesis 28 — Identification of genes periodically expressed in the human cell cycle and their expression in tumors.

Mol Biol Cell 13 — On the road to cancer: aneuploidy and the mitotic checkpoint. Nat Rev Cancer 5 — Siegel JJ, Amon A. New insights into the troubles of aneuploidy. Annu Rev Cell Dev Biol 28 Musacchio A, Salmon ED. The spindle-assembly checkpoint in space and time. Nat Rev Mol Cell Biol 8 — Nasmyth K. Segregating sister genomes: the molecular biology of chromosome separation. Science — Bharadwaj R, Yu H. The spindle checkpoint, aneuploidy, and cancer. Oncogene 23 — Cdc a WD40 activator for a cell cycle degradation machine. Mol Cell 27 :3— Ubiquitination by the anaphase-promoting complex drives spindle checkpoint inactivation.

Nature —5. Determinants of conformational dimerization of Mad2 and its inhibition by p31comet. EMBO J 25 — J Cell Sci — Mutational inactivation of STAG2 causes aneuploidy in human cancer. Overexpressed pituitary tumor-transforming gene causes aneuploidy in live human cells. Endocrinology —8. Overexpression of separase induces aneuploidy and mammary tumorigenesis. Merotelic kinetochore orientation is a major mechanism of aneuploidy in mitotic mammalian tissue cells. J Cell Biol — Cimini D. Merotelic kinetochore orientation, aneuploidy, and cancer.

Biochim Biophys Acta — Saunders W. Centrosomal amplification and spindle multipolarity in cancer cells. Semin Cancer Biol 15 — Peters J-M. Nat Rev Mol Cell Biol 7 — Malumbres M, Barbacid M. Cell cycle kinases in cancer. Curr Opin Genet Dev 17 —5. Mol Cell 35 — Bueno MJ, Malumbres M. MicroRNAs and the cell cycle. Significance of Plk1 regulation by miR in human nasopharyngeal cancer. Int J Cancer — Upregulation of cyclin B1 by miRNA and its implications in cancer.

Nucleic Acids Res 40 — Cell Death Differ 20 — Inhibition of nucleoporin member Nup expression by miRb perturbs mitotic timing and leads to cell death. Mol Cancer 14 A census of human cancer genes. Nat Rev Cancer 4 — Curr Opin Cell Biol 17 — Does aneuploidy cause cancer? Curr Opin Cell Biol 18 — Targeting cell cycle kinases for cancer therapy.

Curr Med Chem 14 — Constitutional aneuploidy and cancer predisposition caused by biallelic mutations in BUB1B. Nat Genet 36 — Cancer Cell 3 — Aurora-A gene is frequently amplified in basal-like breast cancer. Oncol Rep 23 — ECT2 amplification and overexpression as a new prognostic biomarker for early-stage lung adenocarcinoma. Cancer Sci —7. Phenotypic profiling of the human genome by time-lapse microscopy reveals cell division genes.

Nature —7. Is germline transmission of MAD2 gene deletion associated with human fetal loss? Mol Hum Reprod 18 — FEBS J — Dynamic recruitment of NF-Y and histone acetyltransferases on cell-cycle promoters. J Biol Chem — Cell Cycle 6 — Cell Growth Differ 9 — The tumour suppressor protein p53 can repress transcription of cyclin B. Nucleic Acids Res 28 —8. CDC20, a potential cancer therapeutic target, is negatively regulated by p Oncogene 27 — DNA damage induced p53 downregulates Cdc20 by direct binding to its promoter causing chromatin remodeling.

Nucleic Acids Res 37 — FoxM1 is required for execution of the mitotic programme and chromosome stability. Nat Cell Biol 7 — Forkhead box M1 regulates the transcriptional network of genes essential for mitotic progression and genes encoding the SCF Skp2-Cks1 ubiquitin ligase.

  1. Francesca Pentimalli.
  2. Cell Cycle Deregulation in Cancer | Greg H. Enders | Springer.
  3. Groß-Berlin. Analyse der größten Stadterweiterung der Berliner Geschichte (German Edition).

Mol Cell Biol 25 — Plk1-dependent phosphorylation of FoxM1 regulates a transcriptional programme required for mitotic progression. Nat Cell Biol 10 — Mol Cell Biol 21 — Genes Dev 16 — Oncogene 21 — Stevaux O, Dyson NJ. A revised picture of the E2F transcriptional network and RB function. Curr Opin Cell Biol 14 — DeGregori J. The genetics of the E2F family of transcription factors: shared functions and unique roles. The E2F transcriptional network: old acquaintances with new faces. Oncogene 24 — Cam H, Dynlacht BD.

Cancer Cell 3 —6. Rb inactivation promotes genomic instability by uncoupling cell cycle progression from mitotic control. Nature — Mol Endocrinol 23 — Mol Cell Biol 35 — EMBO J 23 — EMBO J 26 — Genome-scale RNAi profiling of cell division in human tissue culture cells.

Nat Cell Biol 9 — Genes Dev 26 — Mol Cell Biol 29 — Biochem Biophys Res Commun — WD repeat-containing mitotic checkpoint proteins act as transcriptional repressors during interphase.

FEBS Lett —9. Spindle assembly checkpoint protein Cdc20 transcriptionally activates expression of ubiquitin carrier protein UbcH PLoS One 7 :e Overexpression of B-type cyclins alters chromosomal segregation. Oncogene 21 —7. Overexpression of cyclin B1 in early-stage non-small cell lung cancer and its clinical implication.

Cancer Res 60 —4. Prognostic value of cyclin B1 in patients with esophageal squamous cell carcinoma. Cancer 94 — Strebhardt K, Ullrich A. Targeting polo-like kinase 1 for cancer therapy. Nat Rev Cancer 6 — Martin BT, Strebhardt K. Polo-like kinase 1: target and regulator of transcriptional control. Cell Cycle 5 —5. Transcriptional regulation of human polo-like kinases and early mitotic inhibitor. J Genet Genomics 35 — Polo-like kinases and oncogenesis.

Human papillomavirus type 16 E6 and E7 cause polyploidy in human keratinocytes and up-regulation of G2-M-phase proteins. Cancer Res 64 — BRCA1 regulates gene expression for orderly mitotic progression.

  • The Hallmarks of Cancer.
  • Oncotarget | The therapeutic potential of cell cycle targeting in multiple myeloma?
  • Cell Cycle targets & Cancer | Malumbres Lab.
  • 1. Introduction.
  • Homage and Honour (Planet Wolf Book 3).
  • chapter and author info.
  • Cell Cycle 4 — Nek2 kinase in chromosome instability and cancer. Cancer Lett — The centrosomal kinase Nek2 displays elevated levels of protein expression in human breast cancer. Cancer Res 64 —6. Cell-cycle-dependent regulation of human aurora A transcription is mediated by periodic repression of E4TF1. Cell cycle-dependent regulation of the human aurora B promoter.

    Biochem Biophys Res Commun —6. Aurora kinases A and B are up-regulated by Myc and are essential for maintenance of the malignant state. Blood — Annual Report to the Nation. Milestones in Cancer Research and Discovery. Stories of Discovery. Terminology Resources. Research Funding Opportunities.

    The Open Clinical Cancer Journal

    Research Program Contacts. Funding Strategy. Grants Policies and Process. Introduction to Grants Process.

    The therapeutic potential of cell cycle targeting in multiple myeloma

    NCI Grant Policies. Legal Requirements. Step 3: Peer Review and Funding Outcomes. Grants Management Contacts. Prior Approvals. Annual Reporting and Auditing. Transfer of a Grant.

    The Hallmarks of Cancer - Wikipedia

    Grant Closeout. Cancer Training at NCI. Resources for Trainees. Funding for Cancer Training. Building a Diverse Workforce. Resources for News Media. Media Contacts. Multicultural Media Outreach Program. Cancer Reporting Fellowships. Advisory Board Meetings. Social Media Events. Cancer Currents Blog. Contributing to Cancer Research. Strategic Planning. Previous NCI Directors. Advisory Boards and Review Groups. NCI Congressional Justification. Current Congress. Legislative History. Committees of Interest.

    Bibliographic Information

    Legislative Resources. Recent Public Laws. Search Search. Adult Treatment. Pediatric Treatment. Adult Treatment Editorial Board. Pediatric Treatment Editorial Board. Cancer Genetics Editorial Board. Integrative Therapies Editorial Board. Levels of Evidence: Treatment. Levels of Evidence: Cancer Genetics. Levels of Evidence: Integrative Therapies. The search textbox has an autosuggest feature. When you enter three or more characters, a list of up to 10 suggestions will popup under the textbox. Use the arrow keys to move through the suggestions.

    To select a suggestion, hit the enter key. Using the escape key closes the listbox and puts you back at the textbox.