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- W2559837447 abstract "Danazol, the established clinical drug, has given promising therapeutic results in a series of clinical trials with breast cancer patients. Danazol shares structural similarities with several known PKC agonists and fits well into the C1 domain. Danazol binds to the C1b domain of PKC with Kd of 5.64 ± 1.27 μm. MD simulation studies further support that the PKC–danazol molecular model is stable and showing minimum distortion to the structure during the simulation period. Immunofluorescence and Western blotting studies indicate that MDAMB-231 cells stimulated with danazol exhibit translocation of PKCα to the plasma membrane. Cells stimulated with danazol causes appearance of several phosphorylated proteins in lysate and plasma membrane. In addition, danazol affects carcinogenic molecule (PMA)-induced intracellular signaling in cancer cells. It halted the cancer cells in the G1 phase of the cell cycle and reduced the viability of ER+ve and triple-negative breast cancer cells with an IC50 of 31 ± 2.63 and 65 ± 4.27 μg/ml, respectively. DNA fragmentation and flow cytometry experiments revealed that the cell death follows the apoptotic pathway. It affects mitochondrial membrane potentials and releases cytochrome-C from mitochondria to induce downstream apoptosis in breast cancer cells. Hence, the current study may help clinicians to re-design their treatment strategy to optimize therapeutic potentials of the molecule." @default.
- W2559837447 created "2016-12-16" @default.
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- W2559837447 date "2017-02-27" @default.
- W2559837447 modified "2023-10-17" @default.
- W2559837447 title "Danazol has potential to cause PKC translocation, cell cycle dysregulation, and apoptosis in breast cancer cells" @default.
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- W2559837447 doi "https://doi.org/10.1111/cbdd.12921" @default.
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