PSME2 May Promote Malignant Progression of Lung Adenocarcinoma via NF-κB Signaling Pathway

This paper combines bioinformatics analysis with in vitro and in vivo studies to investigate the expression profile, prognostic significance, and regulatory mechanisms of PSME2 in lung cancer. Using the TCGA database, we looked at PSME2 expression profiles in lung adenocarcinoma and other cancer types. Additionally, we conducted a correlation study using clinicopathological characteristics; The prognostic significance of PSME2 was evaluated using Kaplan-Meier Plotter. Western blot, immunofluorescence, and immunohistochemistry were employed to verify differences in PSME2 expression between cell lines and clinical tissues. Both temporary PSME2 silencing in A549 cells using siRNA and stable PSME2 knockdown by lentiviral transduction were performed. These results were paired with CCK-8 tests, wound healing assays, Transwell migration assays, and subcutaneous tumor xenograft models in nude mice to validate the regulatory effects of PSME2 on cell proliferation, migration, and invasion both in vitro and in vivo; Western blot analysis is used to quantify the phosphorylation levels of key proteins in order to provide light on the downstream pathways of the NF-κB signaling cascade. The results demonstrated that PSME2 is significantly overexpressed in lung adenocarcinoma tissues and that PSME2 expression levels are significantly correlated with tumor stage, lymph node metastasis, and poor patient prognosis (including decreased overall survival, progression-free survival, and post-progression survival). PSME2 knockdown dramatically decreased the ability of lung adenocarcinoma cells to multiply, move, and invade both in vitro and in vivo. By lowering the phosphorylation levels of significant NF-κB signaling pathway proteins, it also decreased pathway activity. This work indicates that PSME2 is a potential prognostic biomarker and therapeutic target for lung adenocarcinoma since its carcinogenic effects are closely associated with the activation of the NF-κB signaling system.