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ROS-mediated apoptotic cell death in prostate cancer LNCaP cells induced by biosurfactant stabilized CdS quantum dots
Braj R Singh1, Brahma N Singh, W Khan
1Centre of Excellence in Materials Science-Nanomaterials, Department of Applied Physics, Z.H. College of Engg. & Tech., Aligarh Muslim University, Aligarh 202002, Uttar Pradesh, India.
Abstract:
Cadmium sulfide (CdS) quantum dots (QDs) have raised great attention because of their superior optical properties and wide utilization in biological and biomedical studies. However, little is known about the cell death mechanisms of CdS QDs in human cancer cells. This study was designed to investigate the possible mechanisms of apoptosis induced by biosurfactant stabilized CdS QDs (denoted as "bsCdS QDs") in human prostate cancer LNCaP cells. It was also noteworthy that apoptosis correlated with reactive oxygen species (ROS) production, mitochondrial damage, oxidative stress and chromatin condensation in a dose- and time-dependent manner. Results also showed involvement of caspases, Bcl-2 family proteins, heat shock protein 70, and a cell-cycle checkpoint protein p53 in apoptosis induction by bsCdS QDs in LNCaP cells. Moreover, pro-apoptotic protein Bax was upregulated and the anti-apoptotic proteins, survivin and NF-κB were downregulated in bsCdS QDs exposed cells. Protection of N-acetyl cysteine (NAC) against ROS clearly suggested the implication of ROS in hyper-activation of apoptosis and cell death. It is encouraging to conclude that biologically stabilized CdS QDs bear the potential of its applications in biomedicine, such as tumor therapy specifically by inducing caspase-dependent apoptotic cell death of human prostate cancer LNCaP cells.
Insights
Biosurfactant-stabilized cadmium sulfide (CdS) quantum dots (QDs) induce apoptosis in human prostate cancer cells. This cell death mechanism involves reactive oxygen species (ROS) and caspase activation, suggesting potential for tumor therapy.
Area of Science:
- Nanotechnology
- Biomedical Engineering
- Toxicology
Background:
- Cadmium sulfide (CdS) quantum dots (QDs) possess unique optical properties for biomedical applications.
- Mechanisms of CdS QD-induced cell death in human cancer cells remain largely unexplored.
Purpose of the Study:
- Investigate apoptosis mechanisms induced by biosurfactant-stabilized CdS QDs (bsCdS QDs) in human prostate cancer LNCaP cells.
- Elucidate the role of reactive oxygen species (ROS) and key proteins in bsCdS QD-mediated apoptosis.
Main Methods:
- Exposure of LNCaP cells to varying doses and times of bsCdS QDs.
- Assessment of apoptosis markers, ROS production, mitochondrial damage, and protein expression (caspases, Bcl-2 family, p53, survivin, NF-κB).
- Evaluation of N-acetyl cysteine (NAC) protection against ROS.
Main Results:
- bsCdS QDs induced apoptosis in LNCaP cells in a dose- and time-dependent manner.
- Apoptosis correlated with increased ROS, mitochondrial damage, oxidative stress, and chromatin condensation.
- Upregulation of Bax and downregulation of survivin and NF-κB were observed.
- ROS mediated apoptosis, as evidenced by NAC protection.
Conclusions:
- Biosurfactant-stabilized CdS QDs induce caspase-dependent apoptotic cell death in human prostate cancer cells.
- ROS production plays a critical role in bsCdS QD-induced apoptosis.
- bsCdS QDs show potential for tumor therapy applications in biomedicine.
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