肺腺癌（LUAD）的分子靶向治疗取得了重大进展。然而，LUAD的复杂分子模式和高度异质性限制了这些治疗方法的有效性，因此有必要探索LUAD治疗的新靶点。使用基因表达谱数据库分析了LUAD中anillin（ANLN）的表达水平。此外，使用Kaplan-Meier曲线绘制法评估了ANLN基因表达与患者生存结果之间的关联。随后，在A549和H1299细胞系中进行了ANLN的小干扰RNA（siRNA）转染，然后进行了TUNEL、细胞集落形成和Transwell实验，以评估细胞死亡、集落形成和迁移。此外，还进行了Western blot分析，分析ANLN沉默后caspase-1、白细胞介素（IL）-18（IL-18）、IL-1β、NLR家族丝裂原活化蛋白结构域3（NLRP3）、与凋亡相关的具CARD结构域的卵圆球蛋白样蛋白（ASC）和剪切的气孔酸和增殖抑制果胺（GSDMD）的表达水平。结果显示，相比邻近正常样本，LUAD组织中ANLN mRNA的表达显著增加。此外，ANLN的表达水平随着临床分期的推进呈递增趋势。进一步，高ANLN表达水平的患者与低ANLN表达水平的患者相比，整体生存率较低。随后的ANLN沉默实验表明，在A549和H1299细胞中，细胞死亡率增加，集落形成和迁移减少。此外，ANLN沉默导致A549和H1299细胞中与火焰细胞病相关的分子的蛋白表达水平上调，包括caspase-1、NLRP3、剪切的GSDMD、IL-1β、ASC和IL-18。总之，ANLN是LUAD中一个重要的基因和有潜力的治疗靶点。其作为治疗靶点的潜力使其成为进一步探索LUAD新治疗策略的有趣候选者。

Significant advancements have been achieved in the area of molecular targeted therapy for lung adenocarcinoma (LUAD). However, the complex molecular patterns and high heterogeneity of LUAD confine the efficacy of these therapies to a specific subset of patients; therefore, it is necessary to explore novel targets for LUAD treatment. The expression levels of anillin (ANLN) in LUAD were analyzed using the Gene Expression Profiling Interactive Analysis database. Furthermore, the association between ANLN gene expression and patient survival outcomes was evaluated using the Kaplan‑Meier Plotter. Subsequently, small interfering RNA (siRNA) transfection was performed to knock down ANLN in A549 and H1299 cell lines, after which, TUNEL, colony formation and Transwell assays were conducted to assess cell death, colony formation and migration, respectively. Additionally, western blot analysis was performed to analyze the expression levels of caspase‑1, interleukin (IL)‑18 (IL‑18), IL‑1β, NLR family pyrin domain‑containing 3 (NLRP3), apoptosis‑associated speck‑like protein containing a CARD domain (ASC) and cleaved gasdermin D (GSDMD) following ANLN knockdown. The results revealed that ANLN mRNA expression was significantly increased in LUAD tissues compared with adjacent normal samples. Furthermore, the expression levels of ANLN displayed an increasing trend with advancing clinical stage. Furthermore, patients with high ANLN expression levels exhibited poor overall survival rates compared with those with low ANLN expression levels. Subsequent ANLN knockdown experiments indicated elevated cell death rate, and reduced colony formation and migration in both A549 and H1299 cells. Additionally, ANLN knockdown resulted in increased protein expression levels of pyroptosis‑associated molecules, including caspase‑1, NLRP3, cleaved‑GSDMD, IL‑1β, ASC and IL‑18 in both A549 and H1299 cells. In conclusion, ANLN represents an important gene and a promising therapeutic target for LUAD. Its potential as a therapeutic target makes it an interesting candidate for further exploration in the development of novel treatment strategies for LUAD.