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Published on: June 18, 2015
Tamoxifen regulates cell fate through mitochondrial estrogen receptor beta in breast cancer
M Razandi1, A Pedram, V C Jordan
1Division of Endocrinology, Medical Service 111-I, Veterans Affairs Medical Center, Long Beach, CA, USA.
Abstract:
Tamoxifen (TAM) has both cytostatic and cytotoxic properties for breast cancer. TAM engaged mitochondrial estrogen receptor beta (ERβ) as an antagonist in MCF7-BK cells, increasing reactive oxygen species (ROS) concentrations from the mitochondria that were required for cytotoxicity. In part, this derived from TAM downregulating manganese superoxide dismutase (MnSOD) activity by causing the nitrosylation of tyrosine 34, thereby increasing ROS. ROS-activated protein kinase C delta and c-jun N-terminal kinases, resulting in the mitochondrial translocation of Bax and cytochrome C release. Interestingly, TAM failed to cause high ROS levels or induce cell death in MCF7-BK-TR cells due to stimulation of MnSOD activity through agonistic effects at mitochondrial ERβ. In several mouse xenograft models, lentiviral shRNA-induced knockdown of MnSOD caused tumors that grew in the presence of TAM to undergo substantial apoptosis. Tumor MnSOD and mitochondrial ERβ are therefore targets for therapeutic intervention to reverse TAM resistance and enhance a cell death response.
Insights
Tamoxifen resistance in breast cancer involves mitochondrial estrogen receptor beta (ERβ) and manganese superoxide dismutase (MnSOD). Targeting these can restore tamoxifen
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Tamoxifen (TAM) is a crucial breast cancer therapy with cytostatic and cytotoxic effects.
- Mitochondrial estrogen receptor beta (ERβ) plays a role in TAM's mechanism of action.
- Reactive oxygen species (ROS) are implicated in TAM-induced cancer cell death.
Purpose of the Study:
- To investigate the role of mitochondrial ERβ and manganese superoxide dismutase (MnSOD) in TAM resistance.
- To elucidate the mechanisms by which TAM modulates ROS and induces apoptosis.
- To identify potential therapeutic targets for overcoming TAM resistance.
Main Methods:
- Utilized MCF7-BK and MCF7-BK-TR cell lines to study TAM effects.
- Assessed mitochondrial ERβ activity, ROS production, and MnSOD levels.
- Employed lentiviral shRNA to knock down MnSOD in mouse xenograft models.
Main Results:
- TAM acted as an antagonist of mitochondrial ERβ in MCF7-BK cells, increasing ROS and cytotoxicity.
- TAM-induced cytotoxicity was linked to MnSOD downregulation via tyrosine 34 nitrosylation, leading to ROS generation and apoptosis.
- In MCF7-BK-TR cells, agonistic effects on mitochondrial ERβ stimulated MnSOD, preventing ROS increase and cell death.
- Knockdown of MnSOD in mouse xenografts sensitized tumors to TAM, inducing apoptosis.
Conclusions:
- Mitochondrial ERβ and MnSOD activity are critical determinants of TAM sensitivity and resistance in breast cancer.
- TAM resistance can be reversed by targeting tumor MnSOD and mitochondrial ERβ to enhance cell death.
- These findings highlight novel therapeutic strategies for improving breast cancer treatment outcomes.
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