Nitric oxide-dependent cell death in glioblastoma and squamous cell carcinoma via prodeath mitochondrial clustering
View abstract on PubMed
Summary
This summary is machine-generated.Air plasma-activated medium (APAM) and salinomycin induce cancer cell death by increasing nitric oxide (NO), leading to mitochondrial clustering and nuclear damage. This NO-dependent process is crucial for their anticancer effects.
Area Of Science
- Cell Biology
- Biochemistry
- Cancer Research
Background
- Mitochondrial distribution is vital for cell function and survival.
- Monopolar perinuclear mitochondrial clustering (MPMC) is linked to anticancer effects of air plasma-activated medium (APAM).
- Oxidant-dependent tubulin remodeling and mitochondrial fragmentation are associated with MPMC.
Purpose Of The Study
- Investigate the role of nitric oxide (NO) in APAM's anticancer activity.
- Determine the relationship between NO, MPMC, and cell death.
- Explore NO-dependent mechanisms in drug-resistant cancer treatment.
Main Methods
- Time-lapse microscopy to observe NO and MPMC dynamics.
- Measurement of NO, hydroxyl radicals, and lipid peroxides.
- Inhibition of NO using scavengers and augmentation using NO donors.
- Assessment of tubulin remodeling, nuclear damage, and cell death.
Main Results
- APAM treatment increased NO levels and MPMC in cancer cells, but not in normal cells.
- NO scavenging inhibited APAM-induced tubulin remodeling, MPMC, and cell death.
- NO donors enhanced APAM's pro-death effects.
- Salinomycin exhibited similar NO-dependent anticancer effects.
Conclusions
- APAM and salinomycin induce cancer cell death via a NO-dependent pathway.
- MPMC and oxidative mitochondria are critical components of this NO-driven cell death.
- MPMC represents a potential therapeutic target for NO-based anticancer agents against drug-resistant cancers.
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