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Ginsenoside Rg3 sensitizes human non-small cell lung cancer cells to γ-radiation by targeting the nuclear factor-κB
Lei Wang1, Xiankui Li2, Yi-Min Song3
1Department of Respiratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.
Abstract:
At present, it is elusive how non-small cell lung cancer (NSCLC) develops resistance to γ-radiation; however, the transcription factor nuclear factor-κB (NF-κB) and NF-κB-regulated gene products have been proposed as mediators. Ginsenoside Rg3 is a steroidal saponin, which was isolated from Panax ginseng. Ginsenoside Rg3 possesses high pharmacological activity and has previously been shown to suppress NF-κB activation in various types of tumor cell. Therefore, the present study aimed to determine whether Rg3 could suppress NF-κB activation in NSCLC cells and sensitize NSCLC to γ-radiation, using an NSCLC cell line and NSCLC xenograft. A clone formation assay and lung tumor xenograft experiment were used to assess the radiosensitizing effects of ginsenoside Rg3. NF-κB/inhibitor of NF-κB (IκB) modulation was ascertained using an electrophoretic mobility shift assay and western blot analysis. NF-κB-regulated gene products were monitored by western blot analysis. The present study demonstrated that ginsenoside Rg3 was able to sensitize A549 and H1299 lung carcinoma cells to γ-radiation and significantly enhance the efficacy of radiation therapy in C57BL/6 mice bearing a Lewis lung carcinoma cell xenograft tumor. Furthermore, ginsenoside Rg3 suppressed NF-κB activation, phosphorylation of IκB protein and expression of NF-κB-regulated gene products (cyclin D1, c-myc, B-cell lymphoma 2, cyclooxygenase-2, matrix metalloproteinase-9 and vascular endothelial growth factor), a number of which were induced by radiation therapy and mediate radioresistance. In conclusion, the results of the present study suggested that ginsenoside Rg3 may potentiate the antitumor effects of radiation therapy in NSCLC by suppressing NF-κB activity and NF-κB-regulated gene products, leading to the inhibition of tumor progression.
Insights
Ginsenoside Rg3 sensitizes non-small cell lung cancer (NSCLC) to radiation therapy by suppressing nuclear factor-κB (NF-κB) activation. This natural compound enhances antitumor effects by inhibiting key proteins involved in radioresistance and tumor progression.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Non-small cell lung cancer (NSCLC) exhibits resistance to γ-radiation, with nuclear factor-κB (NF-κB) implicated in this process.
- Ginsenoside Rg3, a compound from Panax ginseng, demonstrates anti-tumor properties and inhibits NF-κB activation in various cancer cells.
Purpose of the Study:
- To investigate if ginsenoside Rg3 can suppress NF-κB activation in NSCLC cells.
- To determine if ginsenoside Rg3 can sensitize NSCLC to γ-radiation therapy.
Main Methods:
- Utilized NSCLC cell lines (A549, H1299) and a Lewis lung carcinoma xenograft model in mice.
- Assessed radiosensitizing effects via clone formation assay and xenograft experiments.
- Analyzed NF-κB/inhibitor of NF-κB (IκB) modulation using electrophoretic mobility shift assay and western blot; monitored NF-κB-regulated gene products via western blot.
Main Results:
- Ginsenoside Rg3 sensitized A549 and H1299 NSCLC cells to γ-radiation.
- Demonstrated enhanced radiation therapy efficacy in a murine xenograft model.
- Suppressed NF-κB activation, IκB phosphorylation, and expression of NF-κB-regulated genes (cyclin D1, c-myc, BCL2, COX-2, MMP-9, VEGF) involved in radioresistance.
Conclusions:
- Ginsenoside Rg3 potentiates the antitumor effects of radiation therapy in NSCLC.
- Mechanism involves suppression of NF-κB activity and its downstream gene products, inhibiting tumor progression and overcoming radioresistance.
