An Assessment of InP/ZnS as Potential Anti-Cancer Therapy: Quantum Dot Treatment Increases Apoptosis in HeLa Cells

Abstract

InP/ZnS quantum dots (QDs) are an emerging option in QD technologies for uses of fluorescent imaging as well as targeted drug and anticancer therapies based on their customizable properties. In this study we explored effects of InP/ZnS when treated with HeLa cervical cancer cells. We employed XTT viability assays, reactive oxygen species (ROS) analysis, and apoptosis analysis to better understand cytotoxicity extents at different concentrations of InP/ZnS. In addition, we compared the transcriptome profile from the QD-treated HeLa cells with that of untreated HeLa cells to identify changes to the transcriptome in response to the QD. RT-qPCR assay was performed to confirm the findings of transcriptome analysis, and the QD mode of action was illustrated. Our study determined both IC50 concentration of 69 µg/mL and MIC concentration of 167 µg/mL of InP/ZnS. It was observed via XTT assay that cell viability was decreased significantly at the MIC. Production of superoxide, measured by ROS assay with flow cytometry, was decreased, whereas levels of nitrogen radicals increased. Using analysis of apoptosis, we found that induced cell death in the QD-treated samples was shown to be significantly increased when compared to untreated cells. We conclude InP/ZnS QD to decrease cell viability by inducing stress via ROS levels, apoptosis induction, and alteration of transcriptome.

An antisense amido-bridged nucleic acid gapmer oligonucleotide targeting SRRM4 alters REST splicing and exhibits anti-tumor effects in small cell lung cancer and prostate cancer cells

“…Our preliminary analysis using RT-qPCR showed that low but significant levels of SRRM4 mRNA were expressed in HeLa S3 cells, and the transfection of SRRM4 ASO caused induced caspase3/7 expression. A recent study showed that InP/ZnS quantum dot treatment induced apoptosis, resulting in the downregulation of SRRM4 mRNA in HeLa cells, which prevented tumor growth [ 47 ]. Caspase activation caused by chemically-modified phosphorothioate ASO was previously reported, which correlates with the hepatotoxicity in vivo [ 48 ].…”

Cytotoxicity and Apoptosis-Induction Potential of Fraction F3 from Fruits of Bersama engleriana (Melanthaceae) against Human Cervical Cancer Cells

“…In addition, there was a slight increase in the cell population at the early and late apoptotic stages that correlated with the incubation time. The increase in the population at the early apoptotic stage could be explained by the presence of alterations in membrane asymmetry and pre-lytic DNA fragmentation (Davenport et al, 2021). It is wellknown that early apoptosis involves the activation of multiple signal cascades and can be measured by the presence of Phosphatidylserine (PS) in the outer leaflet of the plasma membrane (detected with annexin V); late apoptosis represents the fragmentation of DNA (Elmore, 2007).…”

Non-ROS-Mediated Cytotoxicity of ZnO and CuO in ML-1 and CA77 Thyroid Cancer Cell Lines

“…ML-1, CA77, and fibroblast cells were maintained in DMEM with 10% FBS, 5% penicillin, and 5% amphotericin. These cell lines were cultured in a CO 2 incubator with 95% O 2 and 5% CO 2 as previously described [ 55 , 56 , 57 ].…”