scholarly journals MiR-205-5p and miR-342-3p cooperate in the repression of the E2F1 transcription factor in the context of anticancer chemotherapy resistance

Theranostics ◽  
2018 ◽  
Vol 8 (4) ◽  
pp. 1106-1120 ◽  
Author(s):  
Xin Lai ◽  
Shailendra K Gupta ◽  
Ulf Schmitz ◽  
Stephan Marquardt ◽  
Susanne Knoll ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Chemotherapy Resistance ◽  
Anticancer Chemotherapy ◽  
E2f1 Transcription Factor

Constitutive expression of the E2F1 transcription factor in fibroblasts alters G0 and S phase transit following serum stimulation

1996 ◽  
Vol 74 (1) ◽  
pp. 21-28 ◽  
Author(s):  
Thomas J. Logan ◽  
Kelly L. Jordan ◽  
David J. Hall
Keyword(s):  
Cell Cycle ◽  
Transcription Factor ◽  
Cell Lines ◽  
Constitutive Expression ◽  
S Phase ◽  
G1 Phase ◽  
Serum Starvation ◽  
Serum Stimulation ◽  
G0 Phase ◽  
E2f1 Transcription Factor

The E2F1 transcription factor was constitutively expressed in NIH3T3 fibroblasts to determine its effect on the cell cycle. These E2F1 cell lines were not tightly synchronized in G0 phase of the cell cycle following serum starvation, as are normal fibroblasts. Instead, the cells are spread throughout G0 and G1 phase with a portion of the population initiating DNA synthesis. Upon serum stimulation, the remaining cells in G0/G1 begin to enter S phase immediately but with a reduced rate. Constitutive expression of E2F1 appears to primarily affect the G0 phase, since transit of proliferating E2F1 cell lines through G1 phase is the same as control cells. Consistent with a shortened G0 phase, the E2F1 cell lines have a significantly reduced cellular volume. Additionally, the first S phase after serum stimulation, but not subsequent S phases, is nearly doubled in the E2F1 cell lines compared with control cells. Cell lines expressing a deletion mutant of E2F1 (termed E2F1d87), known to significantly affect cell shape, have cell cycle and volume characteristics similar to the E2F1 expressing cells. However, all S phase durations are considerably lengthened and the cells demonstrate delayed growth after plating.Key words: cell cycle, E2F1 transcription factor, G0/G1 phase.

E2F1 transcription factor and its impact on growth factor and cytokine signaling

2016 ◽  
Vol 31 ◽  
pp. 17-25 ◽  
Author(s):  
Mustafa Gokhan Ertosun ◽  
Fatma Zehra Hapil ◽  
OZES Osman Nidai
Keyword(s):  
Transcription Factor ◽  
Growth Factor ◽  
Cytokine Signaling ◽  
E2f1 Transcription Factor

scholarly journals Cellular targets for activation by the E2F1 transcription factor include DNA synthesis- and G1/S-regulatory genes.

1995 ◽  
Vol 15 (8) ◽  
pp. 4215-4224 ◽  
Author(s):  
J DeGregori ◽  
T Kowalik ◽  
J R Nevins
Keyword(s):  
Transcription Factor ◽  
Cell Cycle Progression ◽  
Target Genes ◽  
Recombinant Adenovirus ◽  
Cyclin E ◽  
Cyclin A ◽  
S Phase ◽  
Nuclear Antigen ◽  
G1 Arrest ◽  
E2f1 Transcription Factor

Although a number of transfection experiments have suggested potential targets for the action of the E2F1 transcription factor, as is the case for many transcriptional regulatory proteins, the actual targets in their normal chromosomal environment have not been demonstrated. We have made use of a recombinant adenovirus containing the E2F1 cDNA to infect quiescent cells and then measure the activation of endogenous cellular genes as a consequence of E2F1 production. We find that many of the genes encoding S-phase-acting proteins previously suspected to be E2F targets, including DNA polymerase alpha, thymidylate synthase, proliferating cell nuclear antigen, and ribonucleotide reductase, are indeed induced by E2F1. Several other candidates, including the dihydrofolate reductase and thymidine kinase genes, were only minimally induced by E2F1. In addition to the S-phase genes, we also find that several genes believed to play regulatory roles in cell cycle progression, such as the cdc2, cyclin A, and B-myb genes, are also induced by E2F1. Moreover, the cyclin E gene is strongly induced by E2F1, thus defining an autoregulatory circuit since cyclin E-dependent kinase activity can stimulate E2F1 transcription, likely through the phosphorylation and inactivation of Rb and Rb family members. Finally, we also demonstrate that a G1 arrest brought about by gamma irradiation is overcome by the overexpression of E2F1 and that this coincides with the enhanced activation of key target genes, including the cyclin A and cyclin E genes.

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