Coprisin/Compound K Conjugated Gold Nanoparticles Induced Cell Death through Apoptosis and Ferroptosis Pathway in Adenocarcinoma Gastric Cells
- Sanjeevram Dhandapani 1, Abdus Samad 1, Ying Liu 1, Rongbo Wang 1, Sri Renukadevi Balusamy 2, Haribalan Perumalsamy 3,4, Yeon-Ju Kim 1
- Sanjeevram Dhandapani 1, Abdus Samad 1, Ying Liu 1
- 1Graduate School of Biotechnology, and College of Life Science, Kyung Hee University, Yongin-si, Gyeonggi-do 17104, Republic of Korea.
- 2Department of Food Science and Biotechnology, Sejong University, Gwangjin-gu, Seoul 05006, Republic of Korea.
- 3Center for Creative Convergence Education, Hanyang University, Seoul 04763, Republic of Korea.
- 4Research Institute for Convergence of Basic Science, Hanyang University, Seoul 04763, South Korea.
- 0Graduate School of Biotechnology, and College of Life Science, Kyung Hee University, Yongin-si, Gyeonggi-do 17104, Republic of Korea.
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View abstract on PubMed
Summary
This summary is machine-generated.This study reveals that gold nanoparticles combined with compound K and coprisin (GNP-CK-CopA3) effectively induce cancer cell death. The nanomedicine triggers both apoptosis and ferroptosis, offering a dual-targeting strategy against chemoresistant cancers.
Area Of Science
- Biomedical Engineering
- Nanotechnology
- Cancer Biology
Background
- Cancer cells can evade apoptosis through alternative cell death pathways like ferroptosis.
- Targeting dual cell death pathways presents a promising strategy for diverse cancer types.
- Previous work synthesized gold nanoparticles (GNP) with compound K (CK) and coprisin (CopA3) into GNP-CK-CopA3.
Purpose Of The Study
- To assess the anticancer effects of GNP-CK-CopA3 on AGS cells.
- To investigate the induction of apoptosis and ferroptosis by GNP-CK-CopA3.
- To elucidate the underlying molecular mechanisms of GNP-CK-CopA3-induced cell death.
Main Methods
- Cell viability assays and apoptosis induction studies using Hoechst, PI, and Annexin V-FITC/PI staining.
- Mitochondrial disruption and cellular localization analysis via Mito-tracker and transmission electron microscopy.
- Proteomic analysis, molecular docking, and dynamic simulations to identify molecular targets and mechanisms.
Main Results
- GNP-CK-CopA3 demonstrated significant anticancer properties and induced apoptosis in AGS cells.
- Proteomic analysis revealed altered protein expression, highlighting ferroptosis as a key pathway involving GPX4 and GSS.
- Molecular simulations confirmed the binding of CopA3 and CK to GPX4 and GSS, supporting ferroptosis induction.
Conclusions
- GNP-CK-CopA3 exhibits dual-action anticancer properties by inducing both apoptosis and ferroptosis.
- This nanomedicine holds potential as a therapeutic strategy for chemoresistant cancers targeting multiple cell death pathways.
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