scholarly journals 861 CCN2/Connective tissue growth factor regulates G1 to S phase cell cycle progression in human skin fibroblasts

2018 ◽  
Vol 138 (5) ◽  
pp. S146
Author(s):  
T. Quan ◽  
Z. Qin ◽  
T. Purohit ◽  
Y. Shao ◽  
J. Baldassare ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Connective Tissue ◽  
Human Skin ◽  
Cell Cycle Progression ◽  
Tissue Growth ◽  
S Phase ◽  
Phase Cell ◽  
Human Skin Fibroblasts ◽  
Cycle Progression

scholarly journals Stroma-Derived Connective Tissue Growth Factor Maintains Cell Cycle Progression and Repopulation Activity of Hematopoietic Stem Cells In Vitro

2015 ◽  
Vol 5 (5) ◽  
pp. 702-715 ◽  
Author(s):  
Rouzanna Istvánffy ◽  
Baiba Vilne ◽  
Christina Schreck ◽  
Franziska Ruf ◽  
Charlotta Pagel ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Growth Factor ◽  
Connective Tissue ◽  
Hematopoietic Stem Cells ◽  
Cell Cycle Progression ◽  
Tissue Growth ◽  
Cycle Progression ◽  
Hematopoietic Stem

scholarly journals Regulation of Cell Cycle Progression by Growth Factor-Induced Cell Signaling

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3327
Author(s):  
Zhixiang Wang
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Signaling Pathways ◽  
Tyrosine Kinases ◽  
Cell Cycle Progression ◽  
Phase Cell ◽  
Growth Factor Signaling ◽  
Cycle Progression ◽  
M Phase

The cell cycle is the series of events that take place in a cell, which drives it to divide and produce two new daughter cells. The typical cell cycle in eukaryotes is composed of the following phases: G1, S, G2, and M phase. Cell cycle progression is mediated by cyclin-dependent kinases (Cdks) and their regulatory cyclin subunits. However, the driving force of cell cycle progression is growth factor-initiated signaling pathways that control the activity of various Cdk–cyclin complexes. While the mechanism underlying the role of growth factor signaling in G1 phase of cell cycle progression has been largely revealed due to early extensive research, little is known regarding the function and mechanism of growth factor signaling in regulating other phases of the cell cycle, including S, G2, and M phase. In this review, we briefly discuss the process of cell cycle progression through various phases, and we focus on the role of signaling pathways activated by growth factors and their receptor (mostly receptor tyrosine kinases) in regulating cell cycle progression through various phases.

scholarly journals HIV-1 Vif promotes the G1- to S-phase cell-cycle transition

Blood ◽  
2011 ◽  
Vol 117 (4) ◽  
pp. 1260-1269 ◽  
Author(s):  
Jiangfang Wang ◽  
Emma L. Reuschel ◽  
Jason M. Shackelford ◽  
Lauren Jeang ◽  
Debra K. Shivers ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
S Phase ◽  
Phase Cell ◽  
Small Interfering Rnas ◽  
Cycle Progression ◽  
Viral Infectivity Factor ◽  
G2 Phase ◽  
Regulate Cell Cycle Progression ◽  
Hiv 1

AbstractHIV-1 depends on host-cell resources for replication, access to which may be limited to a particular phase of the cell cycle. The HIV-encoded proteins Vpr (viral protein R) and Vif (viral infectivity factor) arrest cells in the G2 phase; however, alteration of other cell-cycle phases has not been reported. We show that Vif drives cells out of G1 and into the S phase. The effect of Vif on the G1-to-S transition is distinct from its effect on G2, because G2 arrest is Cullin5-dependent, whereas the G1-to-S progression is Cullin5-independent. Using mass spectrometry, we identified 2 novel cellular partners of Vif, Brd4 and Cdk9, both of which are known to regulate cell-cycle progression. We confirmed the interaction of Vif and Cdk9 by immunoprecipitation and Western blot, and showed that small interfering RNAs (siRNAs) specific for Cdk9 inhibit the Vif-mediated G1-to-S transition. These data suggest that Vif regulates early cell-cycle progression, with implications for infection and latency.

scholarly journals The RASSF1A Tumor Suppressor Restrains Anaphase-Promoting Complex/Cyclosome Activity during the G1/S Phase Transition To Promote Cell Cycle Progression in Human Epithelial Cells

2008 ◽  
Vol 28 (10) ◽  
pp. 3190-3197 ◽  
Author(s):  
Angelique W. Whitehurst ◽  
Rosalyn Ram ◽  
Latha Shivakumar ◽  
Boning Gao ◽  
John D. Minna ◽  
...  
Keyword(s):  
Phase Transition ◽  
Cell Cycle ◽  
Tumor Suppressor ◽  
Epithelial Cells ◽  
Cyclin D1 ◽  
Cell Cycle Progression ◽  
S Phase ◽  
Phase Cell ◽  
Anaphase Promoting Complex ◽  
Cycle Progression

ABSTRACT Multiple molecular lesions in human cancers directly collaborate to deregulate proliferation and suppress apoptosis to promote tumorigenesis. The candidate tumor suppressor RASSF1A is commonly inactivated in a broad spectrum of human tumors and has been implicated as a pivotal gatekeeper of cell cycle progression. However, a mechanistic account of the role of RASSF1A gene inactivation in tumor initiation is lacking. Here we have employed loss-of-function analysis in human epithelial cells for a detailed investigation of the contribution of RASSF1 to cell cycle progression. We found that RASSF1A has dual opposing regulatory connections to G1/S phase cell cycle transit. RASSF1A associates with the Ewing sarcoma breakpoint protein, EWS, to limit accumulation of cyclin D1 and restrict exit from G1. Surprisingly, we found that RASSF1A is also required to restrict SCFβTrCP activity to allow G/S phase transition. This restriction is required for accumulation of the anaphase-promoting complex/cyclosome (APC/C) inhibitor Emi1 and the concomitant block of APC/C-dependent cyclin A turnover. The consequence of this relationship is inhibition of cell cycle progression in normal epithelial cells upon RASSF1A depletion despite elevated cyclin D1 concentrations. Progression to tumorigenicity upon RASSF1A gene inactivation should therefore require collaborating genetic aberrations that bypass the consequences of impaired APC/C regulation at the G1/S phase cell cycle transition.

scholarly journals Disruption of the Rb-Raf-1 Interaction Inhibits Tumor Growth and Angiogenesis

2004 ◽  
Vol 24 (21) ◽  
pp. 9527-9541 ◽  
Author(s):  
Piyali Dasgupta ◽  
Jiazhi Sun ◽  
Sheng Wang ◽  
Gina Fusaro ◽  
Vicki Betts ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Cell Cycle Progression ◽  
S Phase ◽  
Mitogen Activated Protein Kinase ◽  
Tubule Formation ◽  
Cycle Progression ◽  
Cyclin Dependent Kinases ◽  
Quiescent Cells ◽  
Stimulation Of

ABSTRACT The retinoblastoma tumor suppressor protein (Rb) plays a vital role in regulating mammalian cell cycle progression and inactivation of Rb is necessary for entry into S phase. Rb is inactivated by phosphorylation upon growth factor stimulation of quiescent cells, facilitating the transition from G1 phase to S phase. Although the signaling events after growth factor stimulation have been well characterized, it is not yet clear how these signals contact the cell cycle machinery. We had found previously that growth factor stimulation of quiescent cells lead to the direct binding of Raf-1 kinase to Rb, leading to its inactivation. Here we show that the Rb-Raf-1 interaction occurs prior to the activation of cyclin and/or cyclin-dependent kinases and facilitates normal cell cycle progression. Raf-1-mediated inactivation of Rb is independent of the mitogen-activated protein kinase cascade, as well as cyclin-dependent kinases. Binding of Raf-1 seemed to correlate with the dissociation of the chromatin remodeling protein Brg1 from Rb. Disruption of the Rb-Raf-1 interaction by a nine-amino-acid peptide inhibits Rb phosphorylation, cell proliferation, and vascular endothelial growth factor-mediated capillary tubule formation. Delivery of this peptide by a carrier molecule led to a 79% reduction in tumor volume and a 57% reduction in microvessel formation in nude mice. It appears that Raf-1 links mitogenic signaling to Rb and that disruption of this interaction could aid in controlling proliferative disorders.

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