Owen W. J. Prall

TL;DR: The treatment of MCF-7 breast cancer cells with the pure estrogen antagonist ICI 182780 is treated to inhibit estrogen-induced gene expression and induce G1 phase arrest to provide an explanation for the early activation of both cyclin D1-Cdk4 and cyclin E-C DK2 complexes that accompany G1-S phase progression in response to estradiol.

TL;DR: Examination of clonal MCF-7 breast cancer cell lines provides evidence for distinct c-Myc and cyclin D1 pathways in estrogen-induced mitogenesis which converge on or prior to the formation of active cyclin E-Cdk2-p130 complexes and loss of inactive cycling proteins, indicating a physiologically relevant role for the Cyclin E binding motifs shared by p130 and p21.

TL;DR: It is suggested that lycopene inhibits cell cycle progression via reduction of the cyclin D level and retention of p27 in cyclin E–cdk2, thus leading to inhibition of G1 CDK activities.

TL;DR: These experiments provide compelling evidence that estrogens regulate the expression and function of c-Myc and cyclin D1 and activate cyclin E-Cdk2 complexes, all of which are rate limiting for progression from G1 to S phase.

TL;DR: Treatment of MCF-7 breast cancer cells with the pure estrogen antagonist ICI 182780 results in inhibition of cyclin E-Cdk2 activity prior to a decrease in the G1 to S phase transition, resulting in the arrest of MCf-7 cells in a state with characteristics of quiescence (G0), as opposed to G1 arrest.