1
The estrogen-sensitive MCF-7 breast cancer cell line was used for these studies.
2
It also inhibited the growth of the breast cancer cell line MCF-7.
3
The growth inhibition rate of MCF-7 was increased in a concentration-and time-dependent manner.
4
We aimed to study gene expression profiling circumstances in MCF-7 during MDR development.
5
However, no significant growth inhibition was found between untreated control and RA-treated MCF-10A cells.
6
MCF-7 cells show nuclear as well as cytoplasmic expression of GFP-nCLU in apoptotic cells.
7
RA inhibited the telomerase activity of MCF-7 cells in a wide range of concentrations.
8
MCF-7 cell proliferation was inhibited and autophagy was activated in the same dose-dependent manner.
9
Inhibition of NF-kB activation attenuated irradiated MCF-7-induced tube network formation.
10
The transwell assay was used to measure the invasive capacity of MCF-7 cancer cells.
11
MCF-10 was used as a model of healthy cells.
12
To elucidate the mechanism of action of aminoflavone, we studied DNA damage in MCF-7 cells.
13
Rapid processing may be inherent to PR; it also occurs in PR of MCF-7 cells.
14
It also decreases MAPK activity in TAM-treated MCF-7 cells and in established TR cell lines.
15
Instead, radical oxygen species generation was significantly increased in hirsute and ATM inhibitor-treated MCF-7 cells.
16
The presence or absence of MCF did not correlate with the kinetics of tumor induction.
