Identification of a 51-kilodalton calmodulin binding protein that changes during estrogen-stimulated cell growth

1990 ◽  
Vol 68 (5) ◽  
pp. 863-869 ◽  
Author(s):  
S. Laquerre ◽  
R. Poulin ◽  
F. Labrie ◽  
J. G. Chafouleas

Calmodulin-binding proteins (CaMBPs) were analyzed during estrogen-stimulated growth in the human breast cancer cell line ZR-75-1. A variety of Ca2+-dependent and -independent CaMBPs were observed to be present in these cells. Calmodulin (CaM) binding to a 51-kilodalton protein was shown to be Ca2+-dependent. Moreover, binding to this protein was reduced in the estrogen-treated cells. This effect occurred early during estrogen-stimulated cell growth and was maintained during exponential growth in the presence of estrogen. 125I-labeled CaM overlay procedure of two-dimensional polyacrylamide gels reveals that this 51-kilodalton protein is composed of at least two distinct isoforms with different isoelectric points. Subcellular localization demonstrates that this protein resides exclusively in the microsomal fraction.Key words: calmodulin, calmodulin-binding protein, estrogen-stimulated cell growth.

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Anna Maria Mileo ◽  
Donato Di Venere ◽  
Claudia Abbruzzese ◽  
Stefania Miccadei

Polyphenolic extracts from the edible part of artichoke (Cynara scolymusL.) have been shown to be potential chemopreventive and anticancer dietary compounds. High doses of polyphenolic extracts (AEs) induce apoptosis and decrease the invasive potential of the human breast cancer cell line, MDA-MB231. However, the molecular mechanism underlying AEs antiproliferative effects is not completely understood. We demonstrate that chronic and low doses of AEs treatment at sublethal concentrations suppress human breast cancer cell growth via a caspases-independent mechanism. Furthermore, AEs exposure induces a significant increase of senescence-associatedβ-galactosidase (SA-β-gal) staining and upregulation of tumour suppressor genes,p16INK4aandp21Cip1/Waf1in MDA-MB231 cells. AEs treatment leads to epigenetic alterations in cancer cells, modulating DNA hypomethylation and lysine acetylation levels in total proteins. Cell growth arrest correlates with increased reactive oxygen species (ROS) production in AEs treated breast cancer cells. Inhibition of ROS generation by N-acetylcysteine (NAC) attenuates the antiproliferative effect. These findings demonstrate that chronic AEs treatment inhibits breast cancer cell growth via the induction of premature senescence through epigenetic and ROS-mediated mechanisms. Our results suggest that artichoke polyphenols could be a promising dietary tool either in cancer chemoprevention or/and in cancer treatment as a nonconventional, adjuvant therapy.


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