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Ginsenoside RK1 Induces Ferroptosis in Hepatocellular Carcinoma Cells through an FSP1-Dependent Pathway
Yulang Jiang1,2,3, Yongxin Yu1,2,3, Ziyang Pan1,2,3
1Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.
Background:
Hepatocellular carcinoma (HCC), currently ranking as the third most lethal malignancy, poses a grave threat to human health. Ferroptosis, a form of programmed cell demise, has emerged as a promising therapeutic target in HCC treatment. In this study, we investigated the impact of ginsenoside RK1 on ferroptosis induction in HCC cells and elucidated the underlying mechanisms.
Methods:
The HCC cell line HepG2 was utilized to evaluate the effects of ginsenoside RK1. Distinct dosages of ginsenoside RK1 (25 μM, 50 μM, and 100 μM) were selected based on half-maximal inhibitory concentration (IC50) values. Cellular viability was assessed using a CCK8 assay, cytotoxicity was measured via lactate dehydrogenase (LDH) release assay, and colony-forming ability was evaluated using the clone formation assay. Various inhibitors targeting apoptosis (Z-VAD-FMK 20 μM), necrosis (Nec-1, 10 μM), and ferroptosis (Fer-1, 10 μM; Lip-1, 1 μM) were employed to assess ginsenoside RK1's impact on cell demise. Intracellular levels of key ions, including glutathione (GSH), malondialdehyde (MDA), and iron ions, were quantified, and the protein expression levels of ferroptosis-related genes were evaluated. The sensitivity of HCC cells to ferroptosis induction by ginsenoside RK1 was examined following the overexpression and silencing of the aforementioned target genes.
Results:
Ginsenoside RK1 exhibited an inhibitory effect on HCC cells with an IC50 value of approximately 20 μM. It attenuated cellular viability and colony-forming capacity in a dose-dependent manner, concurrently reducing intracellular GSH levels and increasing intracellular Malondialdehyde (MDA) and iron ion contents. Importantly, cell demise induced by ginsenoside RK1 was specifically counteracted by ferroptosis inhibitors. Furthermore, the modulation of Ferroptosis suppressor protein 1 (FSP1) expression influenced the ability of ginsenoside RK1 to induce ferroptosis. FSP1 overexpression or silencing enhanced or inhibited ferroptosis induction by ginsenoside RK1, respectively.
Conclusions:
Ginsenoside RK1 enhances ferroptosis in hepatocellular carcinoma through an FSP1-dependent pathway.
Insights
Ginsenoside RK1 effectively induces ferroptosis, a cell death pathway, in hepatocellular carcinoma (HCC) cells. This occurs via a mechanism dependent on Ferroptosis suppressor protein 1 (FSP1), offering a potential new therapeutic strategy for HCC.
Area of Science:
- Oncology
- Cell Biology
- Biochemistry
Background:
- Hepatocellular carcinoma (HCC) is a leading cause of cancer mortality worldwide.
- Ferroptosis, a regulated cell death pathway, presents a promising therapeutic target for HCC treatment.
- Ginsenoside RK1 is investigated for its potential to induce ferroptosis in HCC.
Purpose of the Study:
- To investigate the effect of ginsenoside RK1 on ferroptosis induction in HCC cells.
- To elucidate the underlying molecular mechanisms of ginsenoside RK1-induced ferroptosis.
- To evaluate the role of Ferroptosis suppressor protein 1 (FSP1) in this process.
Main Methods:
- Utilized HepG2 HCC cell line and assessed viability, cytotoxicity, and colony formation.
- Employed inhibitors for apoptosis, necrosis, and ferroptosis to determine cell death mechanisms.
- Quantified intracellular levels of glutathione (GSH), malondialdehyde (MDA), and iron ions.
- Evaluated protein expression of ferroptosis-related genes and modulated FSP1 expression.
Main Results:
- Ginsenoside RK1 inhibited HCC cell viability and colony formation in a dose-dependent manner (IC50 ≈ 20 μM).
- RK1 treatment decreased intracellular GSH and increased MDA and iron ion levels, indicative of ferroptosis.
- Cell death induced by ginsenoside RK1 was specifically reversed by ferroptosis inhibitors.
- Modulation of FSP1 expression (overexpression or silencing) significantly affected RK1's ability to induce ferroptosis.
Conclusions:
- Ginsenoside RK1 promotes ferroptosis in hepatocellular carcinoma cells.
- The mechanism of ginsenoside RK1-induced ferroptosis is dependent on Ferroptosis suppressor protein 1 (FSP1).
- This study highlights a potential FSP1-dependent therapeutic strategy for HCC using ginsenoside RK1.
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