Related Experiment Video
Updated: Jan 16, 2026
Establishment of Hepatocarcinoma in BALB/c-nu Mice and Investigation of the Therapeutic Effect of the Sanleng Jiashen Formula
Published on: January 26, 2024
Ginsenosides Enhanced Apoptosis of Serum-Free Starved A549 Lung Cancer Cells
1School of Biological Engineering, Dalian Polytechnic University, Dalian 116034, China.
Abstract:
Lung cancer remains a leading cause of cancer-related mortality worldwide, where conventional chemotherapy is often limited by severe side effects and drug resistance. Ginsenosides, the primary bioactive triterpenoid saponins isolated from the root of Panax ginseng C. A. Mey, have demonstrated potential in combating non-small-cell lung cancer (NSCLC). However, their efficacy under nutrient-deficient conditions remains unclear. This study aimed to investigate the effects of ginsenosides on the growth and death of lung cancer cells under low-nutrient conditions and to explore the underlying mechanisms. A549 cells were divided into two groups: one cultured in 10% serum and another under serum-free conditions, followed by treatment with ginsenosides CK, Rh2(S), and Rg3(S) for 24 h. Cell proliferation and apoptosis were evaluated using a CCK-8 assay, Calcein/PI fluorescence staining, Hoechst 33258 staining, and flow cytometry. Potential targets and signaling pathways of ginsenosides were predicted using network pharmacology and bioinformatics analyses. The mRNA expression of key genes was measured by qRT-PCR, and mitochondrial membrane potential was assessed using JC-1 staining. The results showed that ginsenosides induced dose-dependent apoptosis in serum-starved A549 cells. Bioinformatics analysis suggested the involvement of the PI3K/Akt/FoxO signaling pathway, which was supported by decreased Akt mRNA levels and increased FoxO mRNA expression. Furthermore, mRNA levels of Bim, Caspase-3, Caspase-8, and Caspase-9 were significantly upregulated, accompanied by a loss of mitochondrial membrane potential. These findings indicate that under serum deprivation, ginsenosides enhance apoptosis in A549 cells, likely through the regulation of the PI3K/Akt/FoxO pathway.
Insights
Ginsenosides promote lung cancer cell death under nutrient deprivation by activating apoptosis pathways. This study reveals ginsenosides
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Lung cancer is a major cause of cancer mortality, with chemotherapy facing limitations like drug resistance and severe side effects.
- Ginsenosides from Panax ginseng show promise against non-small-cell lung cancer (NSCLC), but their effectiveness in nutrient-deficient environments is unknown.
Purpose of the Study:
- To investigate the impact of ginsenosides on lung cancer cell growth and apoptosis under low-nutrient conditions.
- To elucidate the molecular mechanisms underlying ginsenoside-induced apoptosis in serum-deprived lung cancer cells.
Main Methods:
- A549 lung cancer cells were cultured in standard (10% serum) and serum-free conditions, treated with ginsenosides (CK, Rh2(S), Rg3(S)).
- Cell proliferation and apoptosis were assessed via CCK-8, Calcein/PI, Hoechst staining, and flow cytometry.
- Network pharmacology, bioinformatics, qRT-PCR, and JC-1 staining were used to analyze signaling pathways and gene expression.
Main Results:
- Ginsenosides induced dose-dependent apoptosis in serum-starved A549 cells.
- Bioinformatics analysis implicated the PI3K/Akt/FoxO pathway; Akt mRNA decreased, FoxO mRNA increased.
- Upregulation of Bim, Caspase-3, -8, -9 mRNA and loss of mitochondrial membrane potential were observed.
Conclusions:
- Ginsenosides enhance apoptosis in lung cancer cells under serum deprivation.
- The PI3K/Akt/FoxO signaling pathway is likely involved in ginsenoside-mediated apoptosis.
