Ginkgetin inhibits the proliferation and migration of lung cancer cells via FAK/STAT3/AKT pathway.

PURPOSE

Lung cancer has become a primary illness that severely endangers human life and health due to its extremely high morbidity and mortality rates. Ginkgetin has been proven to have toxic effects on various tumor cells. Nevertheless, the mechanism of Ginkgetin on lung cancer is uncertain. In the present study, the effect and possible mechanism of Ginkgetin on lung cancer were explored.

METHODS

The cell counting kit-8 assay and colony formation assay were performed to detect the effect of Ginkgetin on cell proliferation. The wound healing assay was performed to detect the effect of Ginkgetin on cell migration. Additionally, western blot and immunofluorescence assay were performed to detect the expression of proteins.

RESULTS

Our results demonstrated that Ginkgetin effectively inhibited the proliferation and migration of A549 and H1299 cells. Mechanistically, Ginkgetin downregulated the phosphorylated expression of focal adhesion kinase (FAK), signal transducer and activator of transcription 3 (STAT3), and protein kinase B (AKT) and blocked the FAK/STAT3/AKT phosphorylation induced by epidermal growth factor (EGF). Furthermore, Ginkgetin suppressed the proliferation and migration of A549 and H1299 cells induced by EGF. Notably, Ginkgetin decreased the Cyclin A2 and Cyclin D1 expression.

CONCLUSION

Collectively, these findings concluded that Ginkgetin may suppress the proliferation and migration of lung cancer cells via the FAK/STAT3/AKT pathway, suggesting that Ginkgetin has potential applications in lung cancer treatment.