Key result
Fat-soluble ginseng components inhibit lung cancer cell growth by up to ~69% and promote apoptosis.
Why the study?
To analyze the regulatory effects and key targets of the fat-soluble components of ginseng in lung cancer.
Do the active fat-soluble components of ginseng inhibit proliferation and promote apoptosis in lung cancer cells?
Do the active fat-soluble components of ginseng inhibit proliferation and promote apoptosis in lung cancer cells?
Absolute Event Rate: 68.5% vs 0%
Fat-soluble components of ginseng demonstrate anti-tumor effects in lung cancer cells in vitro, potentially mediated through the regulation of EGFR, KDR, MAPK3, PTPN11, and CTNNB1 signaling pathways.
Fat-soluble ginseng components inhibit lung cancer cell growth in vitro; hypothesis-generating and should not yet change practice.
OBJECTIVE: To analyze the regulatory effects and key targets of the fat-soluble components of ginseng in lung cancer. METHODS: Gas chromatography-mass spectrometry and the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform were used to analyze and identify the fat-soluble components of ginseng. Network pharmacology was used to analyze the therapeutic targets of the fat-soluble components of ginseng in lung cancer and screen key proteins. In vitro assays were conducted to verify the effects of the active fat-soluble components of ginseng on proliferation and apoptosis in lung cancer cells and to verify the regulation of key proteins. RESULTS: Ten active fat-soluble components of ginseng were screened for follow-up. Network pharmacology showed 33 overlapping targets between the active fat-soluble components of ginseng and lung cancer, and functional enrichment of the targets showed involvement of response to nitrogen, hormone response, membrane raft, and positive regulation of external stimulus. Pathway enrichment analysis showed vascular endothelial growth factor (VEGF) signaling, adipocyte lipolysis regulation, chronic myelogenous leukemia, endocrine resistance, and NSCLC-related pathways. A protein-protein interaction network was constructed, and the top 10 targets were selected in accordance with their scores. Ultimately, five target genes (EGFR, KDR, MAPK3, PTPN11, and CTNNB1) were selected in combination with literature mining for subsequent experimental verification. Proliferation assays showed that the growth of lung cancer cells was significantly decreased in a concentration-dependent manner in the fat-soluble components of ginseng intervention group compared with controls. Flow cytometry showed that active fat-soluble components of ginseng promoted apoptosis in a concentration-dependent manner in lung cancer cells. Western blot and quantitative real-time PCR showed that levels of the five key proteins and mRNAs were significantly decreased in the intervention group; furthermore, histone protein and mRNA levels were significantly higher in the high-concentration intervention group compared with the low-concentration group. CONCLUSION: The active fat-soluble components of ginseng inhibited the growth of lung cancer cells and promoted apoptosis. The underlying regulatory mechanisms may be related to signaling pathways involving EGFR, KDR, MAPK3, PTPN11, and CTNNB1.
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Gao et al. (2023) studied Lung cancer. Fat-soluble components of ginseng vs. Control (0 µg/mL) was evaluated on Cell proliferation inhibition rate in NCI-H1299 cells at 250 µg/mL. The active fat-soluble components of ginseng inhibited the growth of lung cancer cells and promoted apoptosis in a concentration-dependent manner, achieving up to 68.5% growth inhibition at 250 µg/mL.
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