Strategies to target the cancer driver MYC in tumor cells Biology Diagrams An indirect proof of the role of Myc in cell cycle progression is the fact that Mxd proteins (Mxd1, Mxi1, Mxd3, Mxd4 and Mnt), which bind to Myc-binding sites and antagonize Myc transcriptional activity, inhibit cell proliferation (reviewed in [80], [81], [82]). Cell cycle arrest is also observed upon the enforced expression of MadMyc, a
The activation of STAT3 by the cytokine receptor gp130 is required for both the G1 to S cell cycle transition and antiapoptosis. We found that Pim-1 and Pim-2 are targets for the gp130-mediated STAT3 signal. Expression of a kinase-defective Pim-1 mutant attenuated gp130-mediated cell proliferation. Constitutive expression of Pim-1 together with c-myc, another STAT3 target, fully compensated The role of c-Myc in the cell cycle is further highlighted by the marked prolongation of the doubling time of cells in which both alleles of c-myc were eliminated by homologous Shichiri M, Follansbee M R, Sedivy J M. Effects of c-myc expression on cell cycle progression. Mol Cell Biol. 1994;14:5748-5755. doi: 10.1128/mcb.14.9.5748. Induction of cell proliferation by promoting G 1 to S-phase transition during cell cycle progression is one of Myc's best characterized functions, a feature linked to its proโoncogenic
Myc and cell cycle control Biology Diagrams
The entry in cell cycle of quiescent cells upon Myc enforced expression has been described in many models. Also, the downregulation or inactivation of Myc results in the impairment of cell cycle progression. Given the frequent deregulation of Myc oncogene in human cancer it is important to dissect out the mechanisms underlying the role of Myc We further show that heterogeneity in c-Myc dynamics leads to variable target gene transcription and that timing of c-Myc expression predicts cell-cycle progression rates and drug sensitivities. Together, our data advocate for a model in which cancer cells increase the heterogeneity of functionally diverse transcription factors such as c-Myc to
Enforced c-Myc expression promotes inappropriate cell cycle progression of growth factor deprived cells and triggers concomitant apoptosis. However, it is not clear what role dysregulation of the cell cycle plays in c-Myc-induced apoptosis. Ornithine decarboxylase (ODC) is a transcriptional target o โฆ To gain a clearer understanding of the role of c-Myc in cellular proliferation, we have performed a comprehensive analysis of the components that regulate cell cycle progression. The largest defect observed in c-myc-/- cells is a 12-fold reduction in the activity of cyclin D1-Cdk4 and -Cdk6 complexes during the G0-to-S transition. Effects of c-myc expression on cell cycle progression. K D Hanson. K D Hanson. 1 Department of Molecular Biophysics, Yale University School of Medicine, New Dean M., Sonenshein G. E. Cell-cycle control of c-myc but not c-ras expression is lost following chemical transformation. Cell. 1984 Feb;36(2):241-247. doi: 10.1016/0092-8674(84)90217
