Retinoic Acid Inhibition of Cell Cycle Progression in MCF-7 Human Breast Cancer Cells

1997 ◽  
Vol 234 (2) ◽  
pp. 293-299 ◽  
Author(s):  
Wei-Yong Zhu ◽  
Carol S. Jones ◽  
Andras Kiss ◽  
Karen Matsukuma ◽  
Sonal Amin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Retinoic Acid ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Cell Cycle Progression ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Cycle Progression ◽  
Mcf 7

Hormonal regulation of the Grb14 signal modulator and its role in cell cycle progression of MCF-7 human breast cancer cells

2005 ◽  
Vol 203 (1) ◽  
pp. 85-93 ◽  
Author(s):  
Rania Kairouz ◽  
Jayamala Parmar ◽  
Ruth J. Lyons ◽  
Alexander Swarbrick ◽  
Elizabeth A. Musgrove ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Hormonal Regulation ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Cell Cycle Progression ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Cycle Progression ◽  
Mcf 7

scholarly journals Δ9-Tetrahydrocannabinol Inhibits Cell Cycle Progression in Human Breast Cancer Cells through Cdc2 Regulation

2006 ◽  
Vol 66 (13) ◽  
pp. 6615-6621 ◽  
Author(s):  
María M. Caffarel ◽  
David Sarrió ◽  
José Palacios ◽  
Manuel Guzmán ◽  
Cristina Sánchez
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Cell Cycle Progression ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Cycle Progression

scholarly journals Gene expression monitoring in hormone-responsive human breast cancer cells during estrogen-induced cell cycle progression

10.1038/87358 ◽  
2001 ◽  
Vol 27 (S4) ◽  
pp. 95-95
Author(s):  
Luigi Cicatiello ◽  
Angelo Facchiano ◽  
Raffaele Calogero ◽  
Michele De Bortoli ◽  
Francesco Bresciani ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Cell Cycle Progression ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Cycle Progression

scholarly journals Review of: c-Myc suppresses p21WAF1/CIP1expression during oestrogen signalling and antioestrogen resistance in human breast cancer cells

2006 ◽  
Vol 9 (5) ◽  
pp. 1-4
Author(s):  
C. M. McNeil ◽  
E. A. Musgrove
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Cell Cycle Progression ◽  
Human Breast ◽  
Cycle Progression ◽  
Oestrogen Treatment ◽  
Mcf 7

Citation of original article:S. Mukherjee, S. E. Conrad.Journal of Biological Chemistry2005;280: 17616–17625.Abstract of the original article:Oestrogen rapidly induces expression of the proto-oncogene c-Myc. c-Myc is required for oestrogen-stimulated proliferation of breast cancer cells, and deregulated c-Myc expression has been implicated in antioestrogen resistance. In this report, we investigate the mechanism(s) by which c-Myc mediates oestrogen-stimulated proliferation and contributes to cell cycle progression in the presence of antioestrogen. The MCF-7 cell line is a model of oestrogen-dependent, antioestrogen-sensitive human breast cancer. Using stable MCF-7 derivatives with inducible c-Myc expression, we demonstrated that in antioestrogen-treated cells, the elevated mRNA and protein levels of p21WAF1/CIP1, a cell cycle inhibitor, decreased upon either c-Myc induction or oestrogen treatment. Expression of p21 blocked c-Myc-mediated cell cycle progression in the presence of antioestrogen, suggesting that the decrease in p21WAF1/CIP1is necessary for this process. Using RNA interference to suppress c-Myc expression, we further established that c-Myc is required for oestrogen-mediated decreases in p21WAF1/CIP1. Finally, we observed that neither c-Myc nor p21WAF1/CIP1is regulated by oestrogen or antioestrogen in an antioestrogen-resistant MCF-7 derivative. The p21 levels in the antioestrogen-resistant cells increased when c-Myc expression was suppressed, suggesting that loss of p21 regulation was a consequence of constitutive c-Myc expression. Together, these studies implicate p21WAF1/CIP1as an important target of c-Myc in breast cancer cells and provide a link between oestrogen, c-Myc, and the cell cycle machinery. They further suggest that aberrant c-Myc expression, which is frequently observed in human breast cancers, can contribute to antioestrogen resistance by altering p21WAF1/CIP1regulation.

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