Kaempferitrin Regulates the Proliferation, Metastasis, and Immune Escape of Nonsmall Cell Lung Cancer by Inhibiting the Akt/NF-κB Pathway

Nonsmall cell lung cancer (NSCLC) is the most popular type of lung cancer with high morbidity. Kaempferitrin possesses the antitumor effect, while its role in NSCLC development and metastasis remains elusive. Thus, this study aimed to clarify the influence of Kaempferitrin on NSCLC development and elucidate the possible mechanism. In this study, cell viability, apoptosis, invasion, and angiogenesis were assessed using CCK-8, flow cytometry, Transwell invasion, and tube formation assays, respectively. The NF-κB nuclear translocation was observed via Immunofluorescence. In vivo, tumor growth was monitored in a xenograft model, with HE and TUNEL staining assessing tissue damage and apoptosis. Results revealed that Kaempferirin decreased NSCLC cell viability, induced cell apoptosis and suppressed cell motility dose-dependently. Additionally, Kaempferirin restrained the immune escape of NSCLC cells and inactivated the AKT/NF-κB pathway. SC79 could counteract the above effects of Kaempferirin on A549 cells. Moreover, Kaempferirin restrained tumor growth, metastasis and immune escape of NSCLC In vivo. In summary, Kaempferirin inhibited cell proliferation, invasion, angiogenesis, and immune escape and promoted apoptosis of NSCLC by inactivating the AKT/NF-κB pathway. Kaempferirin may be a hopeful drug for NSCLC therapy.