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악성 유방암 세포에서 celastrol 처리시 증가하는 mitochondria 칼슘 이온을 통한 paraptosis 세포 사멸 유도
- Alternative Title
- Celastrol induces paraptosis-like cell death via mitochondrial Ca2+ overload in breast cancer cells
- Author(s)
- Lee, A Reum
- Alternative Author(s)
- A Reum Lee
- Advisor
- 최경숙
- Department
- 일반대학원 의생명과학과
- Publisher
- The Graduate School, Ajou University
- Publication Year
- 2013-08
- Language
- eng
- Keyword
- Breast cancer; Celastrol; Paraptosis; ROS; Ca2+
- Alternative Abstract
- Various cancer cells are resistant to chemotherapeutic drugs-induced apoptosis. Thus, cancer cells that have acquired resistance to apoptosis need novel strategies for inducing non-apoptotic cell death. Paraptosis is a kind of non-apoptotic cell death and characterized by extensive vacuolization due to dilation of mitochondria and the endoplasmic reticulum (ER). However, the regulatory mechanisms that control paraptotic events are not yet fully understood. Recently, we found that celastrol, a triterpene extracted from the Chinese “Thunder of God Vine”, induced paraptosis accompanied by dilation of mitochondria and the ER in MDA-MB 435S and MCF-7 breast cancer cells. Inhibition of protein synthesis by cycloheximide blocked celastrol-induced vacuolation and subsequent cell death indicating that protein synthesis is required for this process. Generation of reactive oxygen species and mitochondrial Ca²⁺ overload was shown to act as a critical early signal in celastrol-induced paraptosis-like cell death contributing to the dilation of mitochondria/ER and subsequent paraptotic cell death. Inhibition of mitochondrial Ca2+ uniporter employing ruthenium red and IP₃ receptor employing 2-APB very effectively blocked celastrol-induced paraptosis-like cell death. Taken together, our results suggest that Ca²⁺ overload into the mitochondria via mitochondrial Ca2+ uniporter and IP3 receptor critically contribute to celastrol-induced paraptosis-like cell death.
- Fulltext
- Appears in Collections:
- Graduate School of Ajou University > Department of Biomedical Sciences > 3. Theses(Master)
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