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.
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Authors | Zahra Shahsavari, Fatemeh Karami-Tehrani, Siamak Salami |
Journal | Asian Pacific journal of cancer prevention : APJCP
(Asian Pac J Cancer Prev)
Vol. 16
Issue 16
Pg. 7261-6
( 2015)
ISSN: 2476-762X [Electronic] Thailand |
PMID | 26514521
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Anti-Inflammatory Agents, Non-Steroidal
- Naphthoquinones
- Reactive Oxygen Species
- shikonin
- Caspase 3
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Topics |
- Anti-Inflammatory Agents, Non-Steroidal
(pharmacology)
- Apoptosis
(drug effects)
- Breast Neoplasms
(drug therapy, metabolism, pathology)
- Caspase 3
(metabolism)
- Cell Proliferation
(drug effects)
- Female
- Humans
- Mitochondria
(drug effects, metabolism)
- Naphthoquinones
(pharmacology)
- Necrosis
- Reactive Oxygen Species
(metabolism)
- Tumor Cells, Cultured
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