Doxorubicin Changes Bax /Bcl-xL Ratio, Caspase-8 and 9 in Breast Cancer Cells

In the present study, we demonstrated that Que postconditioning attenuates myocardial I/R injury in rats via activating the PI3K/Akt pathway and modulating Bcl-2 and Bax

To confirm this hypothesis, we first examined the expression of miR-30c and found that the level of expression was significantly decreased in doxorubicin- resistant cell lines

Dental pulp cells showed increased expression of Bcl-2 and Bax after exposure to high LPS concentrations compared to the control groups and low concentration groups.. The

RESULTS: Prima-1 was able to reactivate p53 function in the T24 (p53 mt) bladder cancer cell line and promote apoptosis via the induction of Bax and Puma expression, activation of

Treatment with EA reduced the number of AF-positive cells in TUNEL staining, increased Bcl-2-positive cells and decreased Bax-positive cells in immunohistochemical

BP-C1 , is significantly reduced cell viability of human breast cancer cells through induction of apoptosis via activation of caspase 8 and caspase 9, increasing the expression

To further characterize the death mechanism of BAX and BAK DKO cells under combined stimulation of ER stress and mild serum withdrawal, cells were treated with a panel of drugs

These observations are consistent with our cytotoxicity results, showing that PrP knockdown in MDA-MB-435 cells has opposite effects on serum deprivation and doxorubicin induced