胃癌（GC）是一种常见的恶性肿瘤，其特征是存活率较低。C型凝集素结构域家族11成员A（CLEC11A）是C型凝集素超家族的一部分，其失调已被认为与多种癌症的进展有关。然而，CLEC11A在GC中的具体作用及其与免疫浸润的关联仍不清楚。本研究中，我们采用了The Cancer Genome Atlas（TCGA）数据库，Gene Expression Omnibus（GEO）数据库，Tumor IMmune Estimation（TIMER）数据库，Gene Expression Profiling Interactive Analysis（GEPIA），UALCAN，Kaplan-Meier绘图器数据库，基因本体（GO），Kyoto Encyclopedia of Genes and Genomes（KEGG），Gene Set Enrichment Analysis（GSEA）和CIBERSORT算法，以研究CLEC11A在GC中的表达、其预后意义、与肿瘤免疫浸润及基因功能富集的关系。我们进行了Western blotting、Cell Counting Kit-8（CCK-8）、伤口愈合和转移试验来验证CLEC11A的功能。我们发现，与癌旁非肿瘤组织相比，GC中CLEC11A的表达显著升高。CLEC11A的高表达与不良生存结局和晚期临床病理分期密切相关。此外，CLEC11A的高表达与免疫调节因子、趋化因子以及GC中免疫细胞（尤其是M2巨噬细胞）的浸润呈正相关。此外，CLEC11A沉默抑制了GC细胞的增殖、迁移和侵袭能力。我们的结果阐明了CLEC11A在GC中的功能，表明它作为一种有价值的GC预后生物标志物和免疫治疗靶点的潜在可能性。

Gastric cancer (GC) is a prevalent malignant cancer characterized by a poor survival rate. The C-type lectin domain family 11 member A (CLEC11A) is part of the C-type lectin superfamily, and its dysregulation has been implicated in the progression of several cancers. The specific role of CLEC11A and its association with immune infiltration in GC, however, remains unclear. In this study, we employed The Cancer Genome Atlas (TCGA) database, Gene Expression Omnibus (GEO) database, Tumor IMmune Estimation Resource (TIMER) database, Gene Expression Profiling Interactive Analysis (GEPIA), UALCAN, Kaplan-Meier plotter databases, gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Set Enrichment Analysis (GSEA), and the CIBERSORT algorithm to investigate CLEC11A expression, its prognostic significance, its association with tumor immune infiltration, and gene function enrichment in GC. We conducted western blotting, Cell Counting Kit-8 (CCK-8), wound healing, and transwell assays to validate CLEC11A's function. We found that CLEC11A expression was significantly elevated in GC when compared to adjacent non-tumor tissues. Elevated CLEC11A expression was strongly associated with poor survival outcomes and advanced clinicopathological stages.  Moreover, heightened CLEC11A expression positively correlated with immunomodulators, chemokines, and the infiltration of immune cells, especially M2 macrophages, in GC. Additionally, CLEC11A silencing suppressed GC cells proliferation, migration and invasion in vitro. Our results elucidate the functions of CLEC11A in GC, suggesting its potential as a valuable prognostic biomarker and therapeutic target for GC immunotherapy.