PIM2 Kinase Inhibitors Affect Lung Cancer through Endoplasmic Reticulum Stress

PIM2 Kinase Inhibitors Affect Lung Cancer through Endoplasmic Reticulum Stress <bold>Background</bold> Lung cancer's high mortality persists despite treatment advances. This study identifies PIM2 kinase as a promising target, exploring its role. <bold>Methods</bold> Using TCGA data, we analyzed PIM2 kinase's expression in lung cancer and its prognostic significance via Kaplan-Meier curves. The inhibitor SMI-16a's effects on lung cancer cell lines were confirmed through CCK8 assays, with apoptosis and proliferation assessed by flow cytometry, and mitochondrial changes via immunofluorescence. Scratch and clone formation assays examined SMI-16a's impact on migration and cloning. Western blotting probed the mechanism by assessing ER stress protein levels, with GraphPad Prism 7.04 for analysis. <bold>Results</bold> High PIM2 kinase levels in lung cancer linked to poor prognosis. SMI-16a inhibited proliferation, promoted apoptosis, and affected mitochondrial potential, slowing migration at low doses. PIM2 inhibition increased endoplasmic stress protein expression, supporting statistical significance. <bold>Conclusion</bold> Increased PIM2 expression in lung cancer indicates poor prognosis. PIM2 inhibition reduced cell proliferation, migration, and clone formation while enhancing apoptosis. The mechanism involves endoplasmic stress, suggesting new therapeutic strategies for lung cancer.