Arsenic Nanoparticles are Effective in Reducing 3-Methylcholanthrene Induced Carcinogenesis in Murine Fibrosarcoma by Promoting Anti-tumorigenic Inflammation

Das, Biswajit; Pal, Anjali; Pal, Ramkrishna; Bodo, Vidisha; Newme, Disuang; Chakraborty, Sayani; Sengupta, Mahuya

doi:10.1007/s12668-021-00920-8

Cited by 3 publications

(1 citation statement)

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“…Several studies have shown that the antiproliferative effects of arsenic on cancer cells are caused by a combination of several factors, such as modulation of intratumoral mitochondrial integrity [ 22 , 30 ] and inflammatory response [ 31 ], reactive oxygen species generation [ 32 ], and the induction of pro-apoptotic genes and suppression of cell death resistance mechanisms [ 33 ]. Regarding skin lesions treatment, there is evidence both in vitro and in vivo that supports the use of arsenic compounds in psoriasis [ 34 ], plantar warts [ 35 ], and melanoma [ 36 ].…”

Section: Introductionmentioning

confidence: 99%

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

Covarrubias,

Reyna-Jeldes,

Pedroso-Santana

et al. 2024

IJMS

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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 Salar de Ascotán, 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 anoikis, an anchorage-dependent type of apoptosis.

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