Sun Longhua, Chen Wen, Yuan Wenxin, Huang Qianwen, Yang Hong, Zhang Wei, Tang Jianjun, Hu Ping
The Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330006, P.R. China.
Jiangxi Provincial Key Laboratory of Respirtory Diseases, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330006, P.R. China.
Mol Biol Rep. 2025 May 14;52(1):458. doi: 10.1007/s11033-025-10540-0.
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.
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.
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.
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.
肺癌因其极高的发病率和死亡率已成为严重危及人类生命健康的主要疾病。白果素已被证明对多种肿瘤细胞具有毒性作用。然而，白果素对肺癌的作用机制尚不清楚。在本研究中，探讨了白果素对肺癌的作用及其可能的机制。
采用细胞计数试剂盒-8法和集落形成试验检测白果素对细胞增殖的影响。采用伤口愈合试验检测白果素对细胞迁移的影响。此外，进行蛋白质免疫印迹和免疫荧光试验检测蛋白质表达。
我们的结果表明，白果素能有效抑制A549和H1299细胞的增殖和迁移。机制上，白果素下调粘着斑激酶（FAK）、信号转导及转录激活因子3（STAT3）和蛋白激酶B（AKT）的磷酸化表达，并阻断表皮生长因子（EGF）诱导的FAK/STAT3/AKT磷酸化。此外，白果素抑制EGF诱导的A549和H1299细胞的增殖和迁移。值得注意的是，白果素降低了细胞周期蛋白A2和细胞周期蛋白D1的表达。
总的来说，这些发现表明白果素可能通过FAK/STAT3/AKT途径抑制肺癌细胞的增殖和迁移，提示白果素在肺癌治疗中具有潜在应用价值。
