Recent studies have revealed that the tumor microenvironment also plays important roles in the development of resistance to therapy. The mechanisms underlying CSC-mediated resistance have been explained from various points of view, such as the expression of multi drug antiporters and slower cell cycle progression of CSC (quiescent/dormant states) in tumors. Multiple studies have consistently reported that the higher resistance capacity of CSCs against chemo- and/or radio-therapies compared to those of non-stem cancer cells significantly contributes to CSC survival after treatment. The current findings provided the basis for further studies on CSC-targeted drugs for the development of cancer treatment strategies.Д¬ancer stem cells (CSCs) are considered to be responsible for various pathological phenomena in cancer, such as tumor initiation, growth, tumor vascularization, recurrence, and metastasis. Moreover, no obvious ICAD reduction/degradation was detected.Д¬onclusion: Daunorubicin effectively eliminated CSCs, which are dependent on the p53/caspase signaling cascade. This was also suppressed by treatment with a Ca 2+-specific chelator, which suggested that CAD endonuclease does not contribute.

Treatment with the caspase inhibitor abolished daunorubicin-induced DNA fragmentation and was therefore considered to act downstream of caspase activation. Daunorubicin-induced apoptosis was found to be associated with p53 accumulation, activation of the caspase cascade, and oligonucleosomal DNA fragmentation. Results: Drug screening studies showed that daunorubicin, a topoisomerase II inhibitor, is specifically cytotoxic to miPS-CSCs. Apoptosis was analyzed by flow cytometry and western blotting. Drug screening was performed on these cells or after transplantation into mice. Methods: CSCs were obtained from mouse induced pluripotent stem cells (miPSCs) using cancer cell-conditioned media. Aim: To identify a drug that can effectively eliminate these cancer stem cells (CSCs) and determine its mode of action.

Icad antibody