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Updated: Jun 3, 2026
Mitochondrial Respiration Quantification in Yeast Whole Cells
Published on: November 8, 2024
Gefitinib induces mitochondrial-dependent apoptosis in Saccharomyces cerevisiae
1Department of Pharmaceutical Engineering, School of Medicine and Pharmaceutics, Jiangnan University, Wuxi, Jiangsu 214122, P.R. China. wujing@jiangnan.edu.cn
Abstract:
Gefitinib, a selective inhibitor of the epidermal growth factor receptor (EGFR) tyrosine kinase, has been clinically demonstrated to be effective in certain cancer cell types. In the present study, using the yeast Saccharomyces cerevisiae as a model, gefitinib-induced apoptotic cell death was demonstrated. Gefitinib inhibited yeast cell proliferation and ultimately led to cell death in a time- and dose-dependent manner. Furthermore, when cells were exposed to 15 µM gefitinib, typical apoptotic markers, including phosphatidylserine exposure, DNA fragmentation, reactive oxygen species production and decrease in mitochondrial membrane potential, were observed. The Δcyc3 strain deleted in cyt c heme lyase and the rho⁰ mutant strain lacking mtDNA-delayed cell death, provided further evidence that the yeast cell death process involved the mitochondria. Thus, these findings suggest that gefitinib induces apoptosis in yeast cells through a mitochondrial-dependent pathway.
Insights
Gefitinib, an EGFR inhibitor, triggers apoptosis in yeast cells. This programmed cell death involves mitochondria and occurs in a time- and dose-dependent manner, offering insights into drug-induced cell death mechanisms.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Gefitinib is an EGFR tyrosine kinase inhibitor effective in certain cancers.
- Yeast models are valuable for studying fundamental cellular processes like apoptosis.
- Understanding drug-induced apoptosis pathways is crucial for therapeutic development.
Purpose of the Study:
- To investigate the effects of gefitinib on yeast cell death.
- To determine if gefitinib induces apoptosis in Saccharomyces cerevisiae.
- To elucidate the role of mitochondria in gefitinib-induced cell death in yeast.
Main Methods:
- Yeast cell proliferation assays.
- Analysis of apoptotic markers (phosphatidylserine exposure, DNA fragmentation, ROS production, mitochondrial membrane potential).
- Utilizing specific yeast strains (Δcyc3, rho⁰ mutant) to assess mitochondrial involvement.
Main Results:
- Gefitinib inhibited yeast cell proliferation and induced cell death.
- Observed typical apoptotic markers at 15 µM gefitinib.
- Mitochondrial involvement was confirmed using specific yeast strains, indicating a mitochondrial-dependent pathway.
Conclusions:
- Gefitinib induces apoptosis in yeast cells.
- The cell death pathway triggered by gefitinib in yeast is mitochondria-dependent.
- This study provides a model for understanding gefitinib's mechanism of action on a cellular level.
