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Ebselen Suppresses Breast Cancer Tumorigenesis by Inhibiting YTHDF1-Mediated c-Fos Expression
Arathy Vasukutty1, Poshan Yugal Bhattarai1, Hong Seok Choi1
1Research Institute of Pharmaceutical Sciences, College of Pharmacy, Chosun University, Gwangju 61452, Republic of Korea.
Abstract:
YTHDF1, an N6-methyladenosine (m6A)-binding protein, plays a key role in breast cancer progression, yet its therapeutic targeting remains underexplored. In this study, we investigated the anticancer effects of the novel YTHDF1 inhibitor ebselen in breast cancer cells. Ebselen treatment reduced cell viability in a dose-dependent manner and induced apoptosis, as demonstrated by Annexin V staining, Sub-G1 accumulation, and DNA fragmentation. Consistently, ebselen increased reactive oxygen species (ROS) production and impaired autophagy induction. Mechanistically, ebselen impaired YTHDF1-mediated stabilization and translation of FOS mRNA, leading to decreased c-Fos expression. In addition, ebselen suppressed anchorage-independent growth in vitro and significantly reduced tumor growth in an orthotopic mouse model. These findings highlight YTHDF1 as a promising therapeutic target and support ebselen as a potential small-molecule inhibitor for breast cancer treatment.
Insights
The YTHDF1 inhibitor ebselen shows promise for breast cancer treatment. Ebselen reduced cancer cell viability, induced apoptosis, and suppressed tumor growth by targeting YTHDF1-mediated FOS mRNA translation.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- YTHDF1, an N6-methyladenosine (m6A)-binding protein, is implicated in breast cancer progression.
- Targeting YTHDF1 presents an underexplored therapeutic strategy for breast cancer.
Purpose of the Study:
- To investigate the anticancer effects of the novel YTHDF1 inhibitor, ebselen, in breast cancer cells.
- To elucidate the underlying molecular mechanisms of ebselen's action.
Main Methods:
- Cell viability assays, Annexin V staining, Sub-G1 accumulation, and DNA fragmentation assays were used to assess apoptosis.
- Reactive oxygen species (ROS) production and autophagy induction were measured.
- FOS mRNA stabilization, translation, and c-Fos expression were analyzed.
- In vitro anchorage-independent growth and in vivo orthotopic mouse models were employed.
Main Results:
- Ebselen treatment reduced breast cancer cell viability and induced apoptosis in a dose-dependent manner.
- Ebselen increased ROS production and impaired autophagy.
- The drug inhibited YTHDF1-mediated FOS mRNA stabilization and translation, decreasing c-Fos expression.
- Ebselen suppressed tumor growth in vitro and in an orthotopic mouse model.
Conclusions:
- YTHDF1 is a viable therapeutic target for breast cancer.
- Ebselen demonstrates significant anticancer activity and warrants further investigation as a potential small-molecule inhibitor for breast cancer treatment.
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