Dataset Information

Silver nanoparticles induces apoptosis of cancer stem cells in head and neck cancer.

ABSTRACT:

Background

Several nano formulations of silver nanoparticles with bioconjugates, herbal extracts and anti-cancerous drug coating have been vividly studied to target cancer. Despite of such extensive studies, AgNPs (silver nanoparticles) have not reached the stage of clinical use. Out of all possible reasons for this failure, the unexplored effect on Cancer Stem Cell (CSC) population and mechanism of action of AgNPs, are the most plausible ones and are worked upon in this study.

Methods

AgNPs were synthesized by chemical reduction method using sodium citrate and characterized by UV, FTIR, XRD and electron microscopy. CSC population was isolated from Cal33 cell line by MACS technique. MTT assay, trypan blue exclusion assay, Annexin V and PI based apoptosis assay and cell cycle assay were performed.

Results

The results showed that synthesized AgNPs have cytotoxic activity on all cancer cell lines tested with the IC₅₀ value of a wide range (1.5-49.21 µg/ml for cell lines and 0.0643-0.1211 µg/ml for splenocytes and thymocytes). CSCs Cal33 showed higher resistance to AgNP treatment and arrest in G1/G0 phase upon cell cycle analysis.

Conclusion

AgNPs as an anti-cancer agent although have great potential but is limited by its off-target effects on normal cells and less effective on cancer stem cells at lower concentrations.

SUBMITTER: Kaur R

PROVIDER: S-EPMC10758978 | biostudies-literature | 2024 Jun

REPOSITORIES: biostudies-literature

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Publications

Silver nanoparticles induces apoptosis of cancer stem cells in head and neck cancer.

Kaur Rupinder R Singh Khushwant K Agarwal Sonam S Masih Marilyn M Chauhan Anita A Gautam Pramod Kumar PK

Toxicology reports 20231128

<h4>Background</h4>Several nano formulations of silver nanoparticles with bioconjugates, herbal extracts and anti-cancerous drug coating have been vividly studied to target cancer. Despite of such extensive studies, AgNPs (silver nanoparticles) have not reached the stage of clinical use. Out of all possible reasons for this failure, the unexplored effect on Cancer Stem Cell (CSC) population and mechanism of action of AgNPs, are the most plausible ones and are worked upon in this study.<h4>Method ...[more]

PMID: 38173651

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Project description:Recent evidence has unveiled a subpopulation of highly tumorigenic, multipotent cells capable of self-renewal in head and neck squamous cell carcinomas (HNSCCs). These unique cells, named here cancer stem cells (CSCs), proliferate slowly and might be involved in resistance to conventional chemotherapy. We have shown that CSCs are found in perivascular niches and rely on endothelial cell-secreted factors [particularly interleukin-6 (IL-6)] for their survival and self-renewal in HNSCC. Here, we hypothesized that cisplatin enhances the stem cell fraction in HNSCC. To address this hypothesis, we generated xenograft HNSCC tumors with University of Michigan-squamous cell carcinoma 22B (UM-SCC-22B) cells and observed that cisplatin treatment increased (P = .0013) the fraction of CSCs [i.e., aldehyde dehydrogenase activity high and cluster of differentiation 44 high (ALDH(high)CD44(high))]. Cisplatin promoted self-renewal and survival of CSCs in vitro, as seen by an increase in the number of orospheres in ultralow attachment plates and induction in B lymphoma Mo-MLV insertion region 1 homolog (Bmi-1) and octamer-binding transcription factor 4 expression. Cisplatin-resistant cells expressed more Bmi-1 than cisplatin-sensitive cells. IL-6 potentiated cisplatin-induced orosphere formation generated when primary human HNSCC cells were sorted for ALDH(high)CD44(high) immediately after surgery and plated onto ultralow attachment plates. IL-6-induced signal transducer and activator of transcription 3 (STAT3) phosphorylation (indicative of stemness) was unaffected by treatment with cisplatin in UM-SCC-22B cells, whereas IL-6-induced extracellular signal-regulated kinase (ERK) phosphorylation (indicative of differentiation processes) was partially inhibited by cisplatin. Notably, cisplatin-induced Bmi-1 was inhibited by interleukin-6 receptor blockade in parental and cisplatin-resistant cells. Taken together, these results demonstrate that cisplatin enhances the fraction of CSCs and suggest a mechanism for resistance to cisplatin therapy in head and neck cancer.

Dataset Information

Silver nanoparticles induces apoptosis of cancer stem cells in head and neck cancer.

Background

Methods

Results

Conclusion

Publications

Silver nanoparticles induces apoptosis of cancer stem cells in head and neck cancer.

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