Anillin (ANLN) encodes one actin-binding protein tightly associated with cell growth, cytokinesis, and migration. The present work focused on exploring differential ANLN expression in lung adenocarcinoma (LUAD). We built an ANLN-related immune prognostic model and verified its feasibility. R and Bioconductor -related software were employed for differential, survival, univariate as well as multivariate analysis. The significance level was P < 0.05. ANLN expression within LUAD tissues was increased compared with non-carcinoma tissues, and ANLN up-regulation in LUAD was associated with poor prognosis. CD8 + T cells showed positive relation to activated CD4 + T cells in LUAD. M2 macrophage abundance was inversely correlated with plasma cell expression. ANLN expression was associated with 17 lymphocytes, 33 immunostimulators, and 13 immunoinhibitors. ANLN-related immunomodulatory genes were mainly involved in cytokine activity, receptor ligand activity, cytokine receptor binding, and tumor necrosis factor receptor binding, and regulated signaling pathways like NF-κB and JAK–STAT pathways. LASSO regression was used to establish an immune risk model. In addition, model prediction performance and feasibility were validated through univariate analysis, multivariate analysis, survival analysis, and ROC curve analysis. Crucially, in vitro experiments demonstrated that ANLN knockdown significantly inhibited the proliferation and migration of A549 and H1299 cells. Mechanistically, ANLN depletion led to the downregulation of NF-κB-related inflammatory cytokines (IL6, CXCL8, and TNF), suggesting a potential role in modulating the tumor immune microenvironment. In conclusion, The ANLN gene is a candidate biomarker for predicting LUAD prognosis, and the constructed risk model may serve as an independent predictor of LUAD prognosis.
Yang et al. (Wed,) studied this question.