Ginsenoside CK Inhibits the Proliferation of Small Cell Lung Cancer Cells and Induces G2/M Cell Cycle Arrest and Apoptosis via the ATM/ATR Signaling Pathway
Objectives: To explore the anti-tumor effect of Ginsenoside compound K (CK) on small cell lung cancer (SCLC). To elucidate the underlying mechanisms of CK's effects on SCLC.
Methods: Investigation through MTT, cell colony formation assays, and AO/EB staining to assess CK’s effect on cell proliferation. Propidium iodide (PI), Annexin V/PI staining, TUNEL assay, and western blotting to analyze CK-induced DNA damage, G2/M arrest, and apoptosis in SCLC cells. A xenograft nude mice model to evaluate the in vivo effect of CK on tumor growth.
Results: CK effectively inhibits the proliferation of SCLC cells in vitro. CK induces DNA damage, G2/M cell cycle arrest, and apoptosis in SCLC cells in a dose-dependent manner. The anti-tumor effects of CK are mediated primarily through the ATM/ATR signaling pathway. In a xenograft model, CK treatment significantly inhibits tumor growth without causing notable side effects.
Conclusion: This study provides the first evidence of CK’s anti-cancer efficacy in SCLC. The findings suggest that CK could be a promising therapeutic approach for SCLC, opening up new opportunities for ginsenosides in lung cancer treatment.
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