Related Experiment Video
Updated: Jan 14, 2026
High-sensitivity Detection of Micrometastases Generated by GFP Lentivirus-transduced Organoids Cultured from a Patient-derived Colon Tumor
Published on: June 14, 2018
Revealing Inhibition of Gastric Cancer Occurrence and Metastasis by GPX3 Through Single-Cell Transcriptomics and
Xing Huang1, Zechen Xiong1, Rong Xue2
1The First Department of General Surgery, Hunan Provincial People's Hospital (The First Affiliated Hospital of Hunan Normal University), Changsha, China.
Abstract:
Metastasis is a major factor leading to an unfavorable prognosis in gastric cancer (GC). However, factors driving GC metastasis are not fully understood. Single-cell transcriptome analysis was done on three primary GC samples, one adjacent nontumor sample, and six GC metastasis samples (GSE163558) to clarify cellular composition characteristics, differential genes, and screen genes related to epithelial-mesenchymal transition (EMT). Effects of GPX3 on GC growth and metastasis were assessed through in vitro cell experiments, a GC liver metastasis model, a GC organoid model, and an organoid xenograft nude mouse model. The primary tumor samples showed a higher proportion of epithelial cells, and analysis revealed a significant reduction in GPX3 levels in GC metastasis samples within the subpopulation of epithelial cells undergoing EMT. Cell experiments demonstrated low expression of GPX3 in GC cells, and overexpression of GPX3 inhibited cell migration, invasion, and EMT in GC cells. Further validation in a nude mouse liver metastasis model confirmed the repressive role of GPX3 in GC metastasis. Additionally, GPX3 could inhibit the growth of patient-derived GC organoids and impede tumor growth and metastasis in an organoid xenograft nude mouse model. This study, based on single-cell transcriptome analysis, revealed the potential inhibitory factor GPX3 in metastatic GC and validated its effects on GC growth and metastasis using GC cells and organoids in vitro and in vivo experiments. These findings offer insights into understanding GC heterogeneity and targeting GPX3 in GC therapeutic strategies.
Insights
Glutathione peroxidase 3 (GPX3) suppresses gastric cancer (GC) metastasis. Overexpressing GPX3 inhibits GC cell migration, invasion, and epithelial-mesenchymal transition (EMT), offering a potential therapeutic target for metastatic GC.
Area of Science:
- Oncology
- Molecular Biology
- Genomics
Background:
- Metastasis significantly worsens gastric cancer (GC) prognosis.
- The molecular drivers of GC metastasis remain incompletely understood.
- Identifying novel therapeutic targets is crucial for improving outcomes in metastatic GC.
Purpose of the Study:
- To investigate the role of GPX3 in GC metastasis using single-cell transcriptome analysis.
- To evaluate the therapeutic potential of GPX3 in inhibiting GC growth and metastasis.
- To clarify the cellular and molecular mechanisms underlying GPX3's function in GC.
Main Methods:
- Single-cell transcriptome analysis of primary and metastatic GC samples.
- In vitro cell experiments assessing migration, invasion, and EMT.
- In vivo studies using GC liver metastasis and organoid xenograft nude mouse models.
- GPX3 expression analysis in epithelial cells undergoing EMT.
Main Results:
- GPX3 levels were significantly reduced in metastatic GC samples, particularly in epithelial cells undergoing EMT.
- Overexpression of GPX3 inhibited GC cell migration, invasion, and EMT.
- GPX3 demonstrated a repressive role in GC liver metastasis in vivo.
- GPX3 inhibited patient-derived GC organoid growth and tumor progression in xenograft models.
Conclusions:
- GPX3 acts as a suppressor of GC growth and metastasis.
- GPX3 holds potential as a therapeutic target for managing metastatic gastric cancer.
- This study provides insights into GC heterogeneity and GPX3's inhibitory mechanisms.
