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Shikonin Induced Necroptosis via Reactive Oxygen Species in the T-47D Breast Cancer Cell Line
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 Title & Authors
Shikonin Induced Necroptosis via Reactive Oxygen Species in the T-47D Breast Cancer Cell Line
Shahsavari, Zahra; Karami-Tehrani, Fatemeh; Salami, Siamak;
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 Abstract
Breast cancer, the most common cancer in the women, is the leading cause of death. Necrotic signaling pathways will enable targeted therapeutic agents to eliminate apoptosis-resistant cancer cells. In the present study, the effect of shikonin on the induction of cell necroptosis or apoptosis was evaluated using the T-47D breast cancer cell line. The cell death modes, caspase-3 and 8 activities and the levels of reactive oxygen species (ROS) were assessed. Cell death mainly occurred through necroptosis. In the presence of Nec-1, caspase-3 mediated apoptosis was apparent in the shikonin treated cells. Shikonin stimulates ROS generation in the mitochondria of T-47D cells, which causes necroptosis or apoptosis. Induction of necroptosis, as a backup-programmed cell death pathway via ROS stimulation, offers a new strategy for the treatment of breast cancer.
 Keywords
Shikonin;ROS;necroptosis;apoptosis;breast cancer;
 Language
English
 Cited by
1.
Shikonin induces glioma cell necroptosis in vitro by ROS overproduction and promoting RIP1/RIP3 necrosome formation, Acta Pharmacologica Sinica, 2017, 38, 11, 1543  crossref(new windwow)
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