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Updated: May 27, 2026
Nanogold Labeling of the Yeast Endosomal System for Ultrastructural Analyses
Published on: July 14, 2014
Identification of the nanogold particle-induced endoplasmic reticulum stress by omic techniques and systems biology
Yen-Yin Tsai1, Yi-Huei Huang, Ya-Li Chao
1Department of Life-Science, Fu-Jen Catholic University, Taipei, Taiwan.
Abstract:
Growth inhibition and apoptotic/necrotic phenotype was observed in nanogold particle (AuNP)-treated human chronic myelogenous leukemia cells. To elucidate the underlying cellular mechanisms, proteomic techniques including two-dimensional electrophoresis/mass spectrometry and protein microarrays were utilized to study the differentially expressed proteome and phosphoproteome, respectively. Systems biology analysis of the proteomic data revealed that unfolded protein-associated endoplasmic reticulum (ER) stress response was the predominant event. Concomitant with transcriptomic analysis using mRNA expression, microarrays show ER stress response in the AuNP-treated cells. The ER stress protein markers' expression assay unveiled AuNPs as an efficient cellular ER stress elicitor. Upon ER stress, cellular responses, including reactive oxygen species increase, mitochondrial cytochrome c release, and mitochondria damage, chronologically occurred in the AuNP-treated cells. Conclusively, this study demonstrates that AuNPs cause cell death through induction of unmanageable ER stress.
Insights
Gold nanoparticles (AuNPs) induce endoplasmic reticulum (ER) stress, leading to cell death in chronic myelogenous leukemia cells. This ER stress response involves reactive oxygen species and mitochondrial damage, ultimately causing apoptosis/necrosis.
Area of Science:
- Nanotechnology
- Cell Biology
- Proteomics
- Cancer Research
Background:
- Human chronic myelogenous leukemia (CML) is a hematological malignancy.
- Nanogold particles (AuNPs) have shown potential in cancer therapy, but their mechanisms of action require elucidation.
- Understanding cellular responses to nanomaterials is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the cellular mechanisms underlying the growth inhibition and apoptotic/necrotic phenotype induced by AuNPs in CML cells.
- To identify key molecular pathways affected by AuNP treatment using proteomic and transcriptomic approaches.
- To determine if endoplasmic reticulum (ER) stress is involved in AuNP-mediated CML cell death.
Main Methods:
- Proteomic analysis using two-dimensional electrophoresis/mass spectrometry to study differential protein expression.
- Protein microarrays to analyze the phosphoproteome.
- Transcriptomic analysis via mRNA expression microarrays.
- Assay of ER stress protein markers.
Main Results:
- Systems biology analysis revealed unfolded protein-associated ER stress response as the predominant event in AuNP-treated CML cells.
- Transcriptomic analysis confirmed ER stress in AuNP-treated cells.
- AuNPs were identified as efficient elicitors of cellular ER stress.
- ER stress triggered reactive oxygen species increase, mitochondrial cytochrome c release, and mitochondrial damage.
Conclusions:
- AuNPs induce cell death in CML cells primarily through the induction of unmanageable ER stress.
- The study elucidates a novel mechanism of AuNP-induced cytotoxicity involving ER stress and subsequent mitochondrial dysfunction.
- These findings highlight the potential of AuNPs as therapeutic agents targeting ER stress pathways in CML.
