MAPKAPK2 (MK2) facilitates the epithelial-mesenchymal transition in lung adenocarcinoma through activation of the AKT/MYC signaling pathway

Purpose The protein kinase Mitogen-Activated Protein Kinase-Activated Protein Kinase 2 (MK2) is linked to higher risks of metastasis and mortality in some cancers. Nonetheless, its precise function in lung adenocarcinoma (LUAD) is still not well understood. Thus, our research focuses on examining MK2’s role within LUAD cells and identifying the underlying mechanisms involved. Methods Differences in MK2 expression among patients with LUAD were confirmed through Timer2.0 database and tissue microarrays. The activity of MK2 in LUAD cell lines A549 and H358 was inhibited using a specific MK2 inhibitor. Thereafter, the viability, migration and mobility were analyzed. Gene expression changes were confirmed through Western blotting. Additionally, an AKT activator was used to validate the role of the MK2-regulated AKT/MYC signaling pathway. Results MK2 shows higher expression in LUAD tissues than in surrounding normal tissues. Reducing MK2 activity not only curtails cell proliferation, migration, and EMT-related invasion in vitro but also disrupts the AKT/MYC signaling axis. Nevertheless, activating the AKT/MYC pathway can counteract the effects of MK2 inhibition. Conclusions Our research shows that MK2 promotes migration and invasion in LUAD through the AKT/MYC signaling pathways, highlighting MK2 as a potential therapeutic target for LUAD.