Stannic Oxide Nanoparticle Regulates Proliferation, Invasion, Apoptosis, and Oxidative Stress of Oral Cancer Cells

Abstract

Objective: To explore the effects of SnO 2 nanoparticles (NPs) on proliferation, invasion, apoptosis, and oxidative stress of oral cancer. Methods: SnO 2 NPs were prepared and characterized. Oral cancer cell lines CAL-27 and SCC-9 were cultured in vitro. We detected the effects of various concentrations of SnO 2 NPs (0, 5, 25, 50, 100, 200 µg/mL) on the proliferation of oral cancer cells, and observed the morphological changes, and measured the cells ability of migration, invasion and apoptosis condition, and the levels of oxidative stress were measured by detecting malondialdehyde (MDA) and reactive oxygen species (ROS). Besides, we also measured the changes of mRNA and protein levels of factors related to cell proliferation, migration, invasion, apoptosis, and oxidative stress. Results: SnO 2 NPs inhibited the proliferation of oral cancer cells in a concentrationdependent manner (all P < 0.05). And SnO 2 NPs treatment could reduce the migration and invasion ability of cells (all P < 0.05), induce apoptosis, and those effects were better when treated for 48 h than 24 h (all P < 0.05). And SnO 2 NPs could induce oxidative stress in cells (all P < 0.05). Besides, the concentrations of cyclin-D1, C-myc, matrix MMP-9, and MMP-2 in SnO 2 NPs treated group was decreased (all P < 0.05), and the expression levels of cleaved Caspase-3, cleaved Caspase-9, and Cytochrome C were increased (all P < 0.05). Conclusion: In the present study, we found that SnO 2 NPs could play a cytotoxic role in oral cancer cells, and inhibit cell proliferation, migration, and invasion, and induce oxidative stress and apoptosis, which suggests that SnO 2 NPs may have the effects of anti-oral cancer. However, a more in-depth study is needed to determine its roles.

Induction of mitochondria mediated apoptosis in human ovarian cancer cells by folic acid coated tin oxide nanoparticles

“…This suggested that oxidative stress is an essential mediator of cytotoxicity induced by SnO 2 NPs and FA-SnO 2 in SKOV3 cells. Similar observation of the overproduction of ROS on time dependent manner in oral cancer cells after treatment with SnO 2 NPs was previously reported [23]. However, other previous study was reported that the effect of SnO 2 NPs against human breast cancer cells was through intracellular ROS increment in dose dependent manner [25].…”

Acute phase response following pulmonary exposure to soluble and insoluble metal oxide nanomaterials in mice

“…[14,30,37] We observed that this NM produces inflammation and induces pulmonary, hepatic and systemic APR in mice, as shown by the increased levels of neutrophils and plasma SAA3, almost as high as our benchmark materials (TiO 2 and Printex 90). In vitro studies with SnO 2 NM have shown that this material decreases cell viability, affects cell membrane structure and increases reactive oxygen species (ROS) production in different cancer cell lines, including a human lung adenorcarcinoma cell line (A549) [69][70][71]. A recent study compared the effects of SnO 2 and TiO 2 NM on A549 cell and murine monocytes.…”

Using Gold-Nanorod-Filled Mesoporous Silica Nanobeads for Enhanced Radiotherapy of Oral Squamous Carcinoma

“…On the other hand, zinc-oxide nanoparticles also showed increased cytotoxicity toward CAL-27 oral cancer cells by PINK1/ Parkin-mediated mitophagy [ 18 ]. Similarly, Li et al found that stannic oxide nanoparticles can exert selective cytotoxic effects on oral cancer cells by inhibiting cell proliferation, migration, and invasion abilities and can also induce oxidative stress and apoptosis [ 37 ]. Although the underlying mechanisms are not fully understood, compatible with previous studies, our results suggest that GNSbs induced selective toxicity toward CAL-27 oral cancer cells.…”