Arsenic Nanoparticles Trigger Apoptosis via Anoikis Induction in OECM-1 Cells

Arsenic compounds have been used as therapeutic alternatives for several diseases including cancer. In the following work, we obtained arsenic nanoparticles (AsNPs) produced by an anaerobic bacterium from the , in northern Chile, and evaluated their effects on the human oral squamous carcinoma cell...

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Veröffentlicht in:International journal of molecular sciences 2024-06, Vol.25 (12), p.6723
Hauptverfasser: Covarrubias, Alejandra A, Reyna-Jeldes, Mauricio, Pedroso-Santana, Seidy, Marín, Sabrina, Madero-Mendoza, Carolina, Demergasso, Cecilia, Coddou, Claudio
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Sprache:eng
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Zusammenfassung:Arsenic compounds have been used as therapeutic alternatives for several diseases including cancer. In the following work, we obtained arsenic nanoparticles (AsNPs) produced by an anaerobic bacterium from the , in northern Chile, and evaluated their effects on the human oral squamous carcinoma cell line OECM-1. Resazurin reduction assays were carried out on these cells using 1-100 µM of AsNPs, finding a concentration-dependent reduction in cell viability that was not observed for the non-tumoral gastric mucosa-derived cell line GES-1. To establish if these effects were associated with apoptosis induction, markers like Bcl2, Bax, and cleaved caspase 3 were analyzed via Western blot, executor caspases 3/7 via luminometry, and DNA fragmentation was analyzed by TUNEL assay, using 100 µM cisplatin as a positive control. OECM-1 cells treated with AsNPs showed an induction of both extrinsic and intrinsic apoptotic pathways, which can be explained by a significant decrease in P-Akt/Akt and P-ERK/ERK relative protein ratios, and an increase in both PTEN and p53 mRNA levels and Bit-1 relative protein levels. These results suggest a prospective mechanism of action for AsNPs that involves a potential interaction with extracellular matrix (ECM) components that reduces cell attachment and subsequently triggers , an anchorage-dependent type of apoptosis.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms25126723