Related Experiment Video
Updated: Jul 2, 2026
Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
Published on: June 9, 2023
Ginsenoside Re Suppresses Tumorigenesis in NSCLC through PERK-Mediated Endoplasmic Reticulum Stress and the
Jiaqi Zhao1, Xinze Liu1, Kaijing Sun1
1Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, 130117, China.
Introduction:
To investigate the antitumor effects of ginsenoside Re on human non-small cell lung cancer cells, specifically the NCI-H460 and 95D cell lines.
Methods:
This study investigated the effects of ginsenoside Re on the proliferation of two cell lines using the CCK-8 assay; observed changes in cell morphology using DAPI and AO/EB staining; analyzed cell cycle and apoptosis rate using flow cytometry; and evaluated cell migration and invasion ability using Transwell and wound healing assays. Western blotting and qPCR results indicated that ginsenoside Re induces apoptosis in NCI-H460 and 95D cells by regulating the expression of genes and proteins, including Bax, BIP, CHOP, eIF-2α, Bcl-2, and β-actin.
Results:
Ginsenoside Re inhibited the proliferation of two cell types in a time- and dosedependent manner. Cell cycle analysis revealed that ginsenoside Re induced G2 phase arrest in NCI-H460 cells and G1/S phase arrest in 95D cells, and that the morphology of apoptosis could be visualized by DAPI and AO/EB fluorescence staining. Cell scratchhealing and invasion assays confirmed that ginsenoside Re inhibited the invasion and migration of NCI-H460 and 95D cells, and the coverage of 95D cells decreased from 73.17±0.26% to 33.02±0.40%.
Discussion:
Ginsenoside Re significantly inhibited NSCLC 95D and NCI-H460 cells by suppressing proliferation, cell cycle progression, migration, invasion, and inducing apoptosis.
Conclusion:
Ginsenoside Re can effectively induce tumor cell apoptosis by regulating the endoplasmic reticulum apoptosis pathway and thereby exert anti-tumor effects. The experiment provides a reliable basis for establishing a mechanistic framework explaining the role of ginsenoside Re in non-small cell lung cancer.
Insights
Ginsenoside Re effectively combats non-small cell lung cancer (NSCLC) by inhibiting tumor cell proliferation, migration, and invasion. It also induces apoptosis through endoplasmic reticulum pathways, offering a promising anti-cancer strategy.
Area of Science:
- Pharmacology
- Oncology
- Molecular Biology
Background:
- Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related mortality.
- Ginsenoside Re, a natural compound, has demonstrated potential anti-cancer properties.
- Investigating its effects on NSCLC cell lines is crucial for therapeutic development.
Purpose of the Study:
- To evaluate the antitumor effects of ginsenoside Re on human NSCLC cell lines (NCI-H460 and 95D).
- To elucidate the mechanisms underlying ginsenoside Re's anti-cancer activity, including apoptosis induction and cell cycle regulation.
Main Methods:
- Cell proliferation was assessed using the CCK-8 assay.
- Apoptosis and cell cycle were analyzed via flow cytometry and DAPI/AO/EB staining.
- Cell migration and invasion were evaluated using Transwell and wound healing assays.
- Western blotting and qPCR were employed to analyze key protein and gene expression.
Main Results:
- Ginsenoside Re inhibited NSCLC cell proliferation in a dose- and time-dependent manner.
- It induced G2 phase arrest in NCI-H460 cells and G1/S phase arrest in 95D cells.
- Ginsenoside Re significantly suppressed cell migration and invasion, with 95D cell coverage decreasing from 73.17% to 33.02%.
Conclusions:
- Ginsenoside Re demonstrates significant anti-NSCLC activity by inhibiting proliferation, cell cycle progression, and metastasis.
- The compound effectively induces apoptosis in NSCLC cells.
- Ginsenoside Re regulates the endoplasmic reticulum apoptosis pathway, providing a mechanistic basis for its anti-tumor effects in NSCLC.
Related Concept Videos
03:03mTOR Signaling and Cancer Progression
The mTOR pathway or the...
01:19Interactions Between Signaling Pathways
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...