Ginsenoside CK ameliorates tumor growth in lung cancer mice via inhibiting EGFR

[Display omitted] •Ginsenoside CK may serve as a potential EGFR tyrosine kinase inhibitor.•Ginsenoside CK suppresses the proliferation and induces the apoptosis of A549 cells.•Ginsenoside CK combined with gefitinib shows better inhibitory effect of tumor growth in mice.•Ginsenoside CK elicits anti-lung cancer effect via the EGFR/MAPK/ERK signaling pathway. In this work, ginsenoside CK was confirmed as an EGFR tyrosine kinase inhibitor, with an IC50 value of 32.58 ± 0.09 μM. Molecular docking showed that ginsenoside CK could fit into EGFR binding pocket, thereby acting as a ligand for EGFR. Ginsenoside CK inhibited proliferation of A549 cells as well as induced its apoptosis via downregulating anti-apoptotic factors and upregulating apoptosis induction factors. Ginsenoside CK alone and combined with gefitinib inhibited the tumor progression of A549 lung cancer xenografts in BALB/c nude mice. ELISA assay showed that ginsenoside CK combined with gefitinib alleviated the inflammatory response by suppressing the release of pro-inflammatory cytokines, indicating better inhibitory effects than ginsenoside CK or gefitinib alone. This work further confirmed that ginsenoside CK regulated the EGFR/MAPK/ERK signaling both in vitro and in vivo. In conclusion, ginsenoside CK can exhibit the anti-lung cancer effect via acting as an EGFR tyrosine kinase inhibitor.