Abstract
Tamoxifen citrate (TAM) has been used to treat breast cancer in women for many years. The com-parative effects of TAM in inducing apoptosis were evaluated in estrogen receptor-positive (ER- positive MCF-7) and estrogen receptor-negative (ER-negative MDA-MB-231) human breast cancer cell lines in vitro in order to determine if these two cell lines differ in their sensitivity to TAM. Mi-tochondrial membrane permeability potential disruption was assessed in both cell lines by a lip-ophilic cationic dye (DePsipher assay, Trevigen, Inc.) utilizing fluorescence microscopy. Using this specific fluorochrome, we were able to associate mitochondrial membrane disruption to early, mid-, and late apoptotic cells. TAM induced cell death via apoptosis in both ER-positive and ER- negative cells, however, apoptosis induction was more pronounced in ER-positive MCF-7 compared to ER-negative MDA-MB-231 breast cancer cells. These findings may have some therapeutic use in the treatment of estrogen dependent and estrogen independent breast cancer.
Highlights
Breast cancer is one of the leading causes of cancer-related deaths in human females, claiming 40,000 lives in 2013 alone [1]
We studied two widely used human breast cancer cell lines, namely estrogen-positive MCF-7 and estrogen-negative MDA-MB-231, to evaluate if these two cell lines differ in their sensitivity to Tamoxifen citrate (TAM) in vitro
Our results revealed that ERα+ MCF-7 cells were statistically more sensitive to TAM treatment compared to ERα-MDA-MB-231 cells as evidenced from collated data obtained by enumerating early, mid- and late apoptotic cells
Summary
Breast cancer is one of the leading causes of cancer-related deaths in human females, claiming 40,000 lives in 2013 alone [1]. (2014) Sensitivity Evaluation of Two Human Breast Cancer Cell Lines to Tamoxifen through Apoptosis Induction. TAM functions as an antagonist of the estrogen receptors of ER-positive (ERα+) breast cancer cells, leading to cell death via apoptosis, and lowering the risk of abnormal cell proliferation in the breast [5] [6]. SERMs function by binding to Estrogen Receptor-alpha (ERα+), resulting in conformational changes in the receptor’s structure [5] [6]. TAM, is more effective in inducing apoptosis in ERα+ breast cancer cells compared to ERα-cells [12] [13]. The ATR-ATM-TP53 pathway, in which the proteins ATR and ATM function, was not found to play a significant role in the Tamoxifen-induced apoptosis of ERα+ cells [16]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
