Title : Premature senescence in human breast cancer and colon cancer cells by tamoxifen-mediated reactive oxygen species generation.

Pub. Date : 2014 Mar 3

PMID : 24361399






5 Functional Relationships(s)
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1 Finally, experiments using T47D (wild-type p53) and MDA-MB-435 (mutant p53) cell lines suggested that tamoxifen induces p53-independent ROS production as well as p53-dependent senescence in breast cancer cells. Tamoxifen tumor protein p53 Homo sapiens
2 Finally, experiments using T47D (wild-type p53) and MDA-MB-435 (mutant p53) cell lines suggested that tamoxifen induces p53-independent ROS production as well as p53-dependent senescence in breast cancer cells. Tamoxifen tumor protein p53 Homo sapiens
3 Finally, experiments using T47D (wild-type p53) and MDA-MB-435 (mutant p53) cell lines suggested that tamoxifen induces p53-independent ROS production as well as p53-dependent senescence in breast cancer cells. Tamoxifen tumor protein p53 Homo sapiens
4 Finally, experiments using T47D (wild-type p53) and MDA-MB-435 (mutant p53) cell lines suggested that tamoxifen induces p53-independent ROS production as well as p53-dependent senescence in breast cancer cells. Tamoxifen tumor protein p53 Homo sapiens
5 SIGNIFICANCE: These results demonstrate that tamoxifen promotes senescence through a ROS-p53-p21(Cip1/WAF1) dependent pathway by inhibiting CK2 activity in breast cancer and colon cancer cells. Tamoxifen tumor protein p53 Homo sapiens