2,3,6- Tribromo- 4,5- dihydroxybenzyl Methyl Ether Induces Growth inhibition and apoptosis in MCF-7 human breast cancer cells

2007 ◽  
Vol 30 (9) ◽  
pp. 1132-1137 ◽  
Author(s):  
Ji-Hyeon Lee ◽  
Sang Eun Park ◽  
Mohammad Akbar Hossain ◽  
Min Young Kim ◽  
Mi-Na Kim ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Methyl Ether ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Mcf 7

Growth inhibition, G1-arrest, and apoptosis in MCF-7 human breast cancer cells by novel highly lipophilic 5-fluorouracil derivatives

2004 ◽  
Vol 22 (4) ◽  
pp. 379-389 ◽  
Author(s):  
Juan Antonio Marchal ◽  
Houria Boulaiz ◽  
Inés Suárez ◽  
Estrella Saniger ◽  
Joaquín Campos ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
G1 Arrest ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Mcf 7

scholarly journals Sphingosine Kinase Transmits Estrogen Signaling in Human Breast Cancer Cells

2003 ◽  
Vol 17 (10) ◽  
pp. 2002-2012 ◽  
Author(s):  
Olga A. Sukocheva ◽  
Lijun Wang ◽  
Nathaniel Albanese ◽  
Stuart M. Pitson ◽  
Mathew A. Vadas ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Sphingosine Kinase ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Mcf 7 ◽  
Cytoplasmic Signaling

Abstract Current understanding of cytoplasmic signaling pathways that mediate estrogen action in human breast cancer is incomplete. Here we report that treatment with 17β-estradiol (E2) activates a novel signaling pathway via activation of sphingosine kinase (SphK) in MCF-7 breast cancer cells. We found that E2 has dual actions to stimulate SphK activity, i.e. a rapid and transient activation mediated by putative membrane G protein-coupled estrogen receptors (ER) and a delayed but prolonged activation relying on the transcriptional activity of ER. The E2-induced SphK activity consequently activates downstream signal cascades including intracellular Ca2+ mobilization and Erk1/2 activation. Enforced expression of human SphK type 1 gene in MCF-7 cells resulted in increases in SphK activity and cell growth. Moreover, the E2-dependent mitogenesis were highly promoted by SphK overexpression as determined by colony growth in soft agar and solid focus formation. In contrast, expression of SphKG82D, a dominant-negative mutant SphK, profoundly inhibited the E2-mediated Ca2+ mobilization, Erk1/2 activity and neoplastic cell growth. Thus, our data suggest that SphK activation is an important cytoplasmic signaling to transduce estrogen-dependent mitogenic and carcinogenic action in human breast cancer cells.

Sign in / Sign up

Export Citation Format

Share Document