Abstract

Lung adenocarcinoma is known to be a malignancy and a leading contributor to mortality. This research intended to delve into the impact of various dosages of gemcitabine on lung adenocarcinoma A549 and PC-9 cells proliferation, migration, and invasion. Additionally, the possible underlying mechanisms were also examined. An in vitro cell model was utilized in the experiment. Varying doses of gemcitabine (2.5, 5, 10 μM) were administered for treating A549 and PC-9 for 0 h-96 h. 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyl tetrazolium bromide determined the half-maximal inhibitory concentration of gemcitabine in A549 and PC- 9. The experiment of cell counting kit-8 assayed cell proliferation and flow cytometry tracked cell apoptosis. The assay of Transwell examined cell migration and invasion. Furthermore, the analysis of Western blot gauged the profiles of apoptotic proteins c-caspase 3 and B-cell lymphoma 2-associated X protein, the antiapoptotic protein B-cell lymphoma 2, and the Janus tyrosine kinase 2/signal transducer and activator of the transcription 3 signaling pathway in A549 and PC-9. As suggested by our findings, gemcitabine dampened proliferation, invasion, and migration while boosting apoptosis in the cells of A549 and PC-9. Further investigations unveiled that gemcitabine impeded Janus tyrosine kinase 2/signal transducer and activator of the transcription 3 signaling pathway activation in these cells. To conclude, this research has corroborated that gemcitabine exerts inhibitory effects on A549 and PC-9 cells’ proliferation, invasion, and migration capabilities by repressing Janus tyrosine kinase 2/signal transducer and activator of the transcription 3 signaling pathway activation under lung adenocarcinoma conditions.