scholarly journals Tumor Suppressors RB1 and CDKN2a Cooperatively Regulate Cell-Cycle Progression and Differentiation During Cardiomyocyte Development and Repair

2019 ◽  
Vol 124 (8) ◽  
pp. 1184-1197 ◽  
Author(s):  
Konstantinos E. Hatzistergos ◽  
Adam R. Williams ◽  
Derek Dykxhoorn ◽  
Michael A. Bellio ◽  
Wendou Yu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Tumor Suppressors ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Regulate Cell Cycle Progression

scholarly journals Inactivation of CtIP Leads to Early Embryonic Lethality Mediated by G1 Restraint and to Tumorigenesis by Haploid Insufficiency

2005 ◽  
Vol 25 (9) ◽  
pp. 3535-3542 ◽  
Author(s):  
Phang-Lang Chen ◽  
Feng Liu ◽  
Suna Cai ◽  
Xiaoqin Lin ◽  
Aihua Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Transcriptional Repression ◽  
Cell Cycle Progression ◽  
Tumor Formation ◽  
3T3 Cells ◽  
Embryonic Fibroblasts ◽  
Cycle Progression ◽  
Early Embryonic Lethality ◽  
Nih 3T3 ◽  
Regulate Cell Cycle Progression

ABSTRACT CtIP interacts with a group of tumor suppressor proteins including RB (retinoblastoma protein), BRCA1, Ikaros, and CtBP, which regulate cell cycle progression through transcriptional repression as well as chromatin remodeling. However, how CtIP exerts its biological function in cell cycle progression remains elusive. To address this issue, we generated an inactivated Ctip allele in mice by inserting a neo gene into exon 5. The corresponding Ctip − / − embryos died at embryonic day 4.0 (E4.0), and the blastocysts failed to enter S phase but accumulated in G1, leading to a slightly elevated cell death. Mouse NIH 3T3 cells depleted of Ctip were arrested at G1 with the concomitant increase in hypophosphorylated Rb and Cdk inhibitors, p21. However, depletion of Ctip failed to arrest Rb − / − mouse embryonic fibroblasts (MEF) or human osteosarcoma Saos-2 cells at G1, suggesting that this arrest is RB dependent. Importantly, the life span of Ctip +/ − heterozygotes was shortened by the development of multiple types of tumors, predominantly, large lymphomas. The wild-type Ctip allele and protein remained detectable in these tumors, suggesting that haploid insufficiency of Ctip leads to tumorigenesis. Taken together, this finding uncovers a novel G1/S regulation in that CtIP counteracts Rb-mediated G1 restraint. Deregulation of this function leads to a defect in early embryogenesis and contributes, in part, to tumor formation.

scholarly journals Circadian regulation of c-MYC in mice

2020 ◽  
Vol 117 (35) ◽  
pp. 21609-21617
Author(s):  
Zhenxing Liu ◽  
Christopher P. Selby ◽  
Yanyan Yang ◽  
Laura A. Lindsey-Boltz ◽  
Xuemei Cao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Circadian Clock ◽  
Tumor Suppressors ◽  
Feedback Loop ◽  
Cell Cycle Progression ◽  
Regulatory Mechanism ◽  
Clock Genes ◽  
Circadian Regulation ◽  
Cycle Progression ◽  
Insight Into

The circadian clock is a global regulatory mechanism that controls the expression of 50 to 80% of transcripts in mammals. Some of the genes controlled by the circadian clock are oncogenes or tumor suppressors. Among theseMychas been the focus of several studies which have investigated the effect of clock genes and proteins onMyctranscription and MYC protein stability. Other studies have focused on effects ofMycmutation or overproduction on the circadian clock in comparison to their effects on cell cycle progression and tumorigenesis. Here we have used mice with mutations in the essential clock genesBmal1,Cry1,andCry2to gain further insight into the effect of the circadian clock on this important oncogene/oncoprotein and tumorigenesis. We find that mutation of bothCry1andCry2, which abolishes the negative arm of the clock transcription–translation feedback loop (TTFL), causes down-regulation of c-MYC, and mutation ofBmal1,which abolishes the positive arm of TTFL, causes up-regulation of the c-MYC protein level in mouse spleen. These findings must be taken into account in models of the clock disruption–cancer connection.

scholarly journals The homeoprotein DLX3 and tumor suppressor p53 co-regulate cell cycle progression and squamous tumor growth

Oncogene ◽  
2015 ◽  
Vol 35 (24) ◽  
pp. 3114-3124 ◽  
Author(s):  
E Palazzo ◽  
M Kellett ◽  
C Cataisson ◽  
A Gormley ◽  
P W Bible ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Tumor Suppressor ◽  
Tumor Growth ◽  
Cell Cycle Progression ◽  
Tumor Suppressor P53 ◽  
Cycle Progression ◽  
Regulate Cell Cycle Progression

scholarly journals B Lymphocytes Differentially Use the Rel and Nuclear Factor κB1 (NF-κB1) Transcription Factors to Regulate Cell Cycle Progression and Apoptosis in Quiescent and Mitogen-activated Cells

1998 ◽  
Vol 187 (5) ◽  
pp. 663-674 ◽  
Author(s):  
Raelene J. Grumont ◽  
Ian J. Rourke ◽  
Lorraine A. O'Reilly ◽  
Andreas Strasser ◽  
Kensuke Miyake ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Transcription Factors ◽  
B Cells ◽  
B Cell ◽  
B Lymphocytes ◽  
Cell Cycle Progression ◽  
Nuclear Factor ◽  
Cycle Progression ◽  
Regulate Cell Cycle Progression

Rel and nuclear factor (NF)-κB1, two members of the Rel/NF-κB transcription factor family, are essential for mitogen-induced B cell proliferation. Using mice with inactivated Rel or NF-κB1 genes, we show that these transcription factors differentially regulate cell cycle progression and apoptosis in B lymphocytes. Consistent with an increased rate of mature B cell turnover in naive nfkb1−/− mice, the level of apoptosis in cultures of quiescent nfkb1−/−, but not c-rel−/−, B cells is higher. The failure of c-rel−/− or nfkb1−/− B cells to proliferate in response to particular mitogens coincides with a cell cycle block early in G1 and elevated cell death. Expression of a bcl-2 transgene prevents apoptosis in resting and activated c-rel−/− and nfkb1−/− B cells, but does not overcome the block in cell cycle progression, suggesting that the impaired proliferation is not simply a consequence of apoptosis and that Rel/NF-κB proteins regulate cell survival and cell cycle control through independent mechanisms. In contrast to certain B lymphoma cell lines in which mitogen-induced cell death can result from Rel/NF-κB–dependent downregulation of c-myc, expression of c-myc is normal in resting and stimulated c-rel−/− B cells, indicating that target gene(s) regulated by Rel that are important for preventing apoptosis may differ in normal and immortalized B cells. Collectively, these results are the first to demonstrate that in normal B cells, NF-κB1 regulates survival of cells in G0, whereas mitogenic activation induced by distinct stimuli requires different Rel/NF-κB factors to control cell cycle progression and prevent apoptosis.

Mitf cooperates with Rb1 and activates p21Cip1 expression to regulate cell cycle progression

Nature ◽  
2005 ◽  
Vol 433 (7027) ◽  
pp. 764-769 ◽  
Author(s):  
Suzanne Carreira ◽  
Jane Goodall ◽  
Isil Aksan ◽  
S. Anna La Rocca ◽  
Marie-Dominique Galibert ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Regulate Cell Cycle Progression

Epigenetic dynamics across the cell cycle

2010 ◽  
Vol 48 ◽  
pp. 107-120 ◽  
Author(s):  
Tony Bou Kheir ◽  
Anders H. Lund
Keyword(s):  
Cell Cycle ◽  
Chromosome Segregation ◽  
Cell Cycle Progression ◽  
Current Knowledge ◽  
Chromatin Condensation ◽  
Chromatin Modifications ◽  
Cycle Progression ◽  
Daughter Cells ◽  
Mammalian Cell Cycle ◽  
Regulate Cell Cycle Progression

Progression of the mammalian cell cycle depends on correct timing and co-ordination of a series of events, which are managed by the cellular transcriptional machinery and epigenetic mechanisms governing genome accessibility. Epigenetic chromatin modifications are dynamic across the cell cycle, and are shown to influence and be influenced by cell-cycle progression. Chromatin modifiers regulate cell-cycle progression locally by controlling the expression of individual genes and globally by controlling chromatin condensation and chromosome segregation. The cell cycle, on the other hand, ensures a correct inheritance of epigenetic chromatin modifications to daughter cells. In this chapter, we summarize the current knowledge on the dynamics of epigenetic chromatin modifications during progression of the cell cycle.

scholarly journals FOXO target gene CTDSP2 regulates cell cycle progression through Ras and p21Cip1/Waf1

2015 ◽  
Vol 469 (2) ◽  
pp. 289-298 ◽  
Author(s):  
David E.A. Kloet ◽  
Paulien E. Polderman ◽  
Astrid Eijkelenboom ◽  
Lydia M. Smits ◽  
Miranda H. van Triest ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Kinase Inhibitor ◽  
Cyclin Dependent Kinase ◽  
Cycle Progression ◽  
Cyclin Dependent Kinase Inhibitor ◽  
Altered Gene Expression ◽  
Forkhead Box ◽  
Altered Gene ◽  
Regulate Cell Cycle Progression

Growth factor controlled activity of forkhead box O transcription factors results in altered gene expression, including expression of CTDSP2 (C-terminal domain small phosphatase 2). CTDSP2 can regulate cell cycle progression through Ras and the cyclin-dependent kinase inhibitor p21Cip1/Waf1.

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