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Updated: Oct 18, 2025

In Vitro and In Vivo Detection of Mitophagy in Human Cells, C. Elegans, and Mice
Published on: November 22, 2017
The prohibitin-binding compound fluorizoline inhibits mitophagy in cancer cells
Sonia Núñez-Vázquez1,2,3, José Saura-Esteller1, Ismael Sánchez-Vera1
1Departament de Ciències Fisiològiques, Facultat de Medicina i Ciències de la Salut, Universitat de Barcelona, Oncobell-IDIBELL (Institut d'Investigació Biomèdica de Bellvitge), L'Hospitalet de Llobregat, Barcelona, Spain.
Abstract:
Fluorizoline is a prohibitin-binding compound that triggers apoptosis in several cell lines from murine and human origin, as well as in primary cells from hematologic malignancies by inducing the integrated stress response and ER stress. Recently, it was described that PHB (Prohibitin) 1 and 2 are crucial mitophagy receptors involved in mediating the autophagic degradation of mitochondria. We measured mitophagy in HeLa cells expressing Parkin and in A549, a lung cancer cell line that can undergo mitophagy in a Parkin-independent manner, and we demonstrated that both fluorizoline and rocaglamide A, another PHB-binding molecule, inhibit CCCP- and OA-induced mitophagy. Moreover, we demonstrated that PHBs are mediating Parkin-dependent mitophagy. In conclusion, besides being a potent pro-apoptotic compound, we present fluorizoline as a promising new mitophagy modulator that could be used as anticancer agent.
Insights
Fluorizoline, a prohibitin-binding compound, induces apoptosis and inhibits mitophagy. This dual action suggests fluorizoline
Area of Science:
- Cell Biology
- Molecular Oncology
- Autophagy Research
Background:
- Prohibitin (PHB) 1 and 2 are identified as key mitophagy receptors.
- Mitochondrial degradation via mitophagy is crucial for cellular homeostasis.
- PHB-binding compounds offer potential therapeutic avenues.
Purpose of the Study:
- To investigate the effect of fluorizoline on mitophagy.
- To explore the role of prohibitin (PHB) in mitophagy.
- To evaluate fluorizoline as a potential anticancer agent.
Main Methods:
- Measuring mitophagy in HeLa and A549 cell lines.
- Utilizing Parkin-expressing cells and Parkin-independent mitophagy models.
- Assessing the impact of fluorizoline and rocaglamide A on mitophagy induction.
Main Results:
- Fluorizoline and rocaglamide A inhibit mitophagy.
- Prohibitins (PHBs) mediate Parkin-dependent mitophagy.
- Fluorizoline demonstrates dual action: pro-apoptotic and mitophagy modulation.
Conclusions:
- Fluorizoline is a potent pro-apoptotic agent.
- Fluorizoline acts as a novel mitophagy modulator.
- Fluorizoline shows promise as an anticancer therapeutic agent.
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