背景：Abelson相互作用子家族成员3（ABI3）编码的蛋白质不仅能抑制肿瘤细胞的异位转移，还能阻碍其迁移。尽管已发现 ABI3 可以调节多种肿瘤的进展，但尚未对其影响进行全面的泛癌分析。方法：从基因组数据共享（GDC）数据门户和 UCSC XENA 数据库检索肿瘤和正常组织的转录组学数据。为了收集 ABI3 的蛋白质信息，利用了人类蛋白质图谱 (HPA) 和 GeneMANIA 网站。此外，还参考了肿瘤免疫单细胞中心 (TISCH) 数据库来确定癌症微环境中表达 ABI3 的主要细胞类型。利用单变量 Cox 回归方法来评估 ABI3 在癌症中的预后作用。利用 Cbioportal 和基因集癌症分析 (GSCA) 网站来仔细检查癌症的基因组图谱信息。利用 TIMER2.0 来探测与 ABI3 相关的跨癌症免疫细胞浸润。通过Spearman相关法分析ABI3与免疫相关基因的关联。利用基因集富集分析（GSEA）和基因集变异分析（GSVA）来搜索相关的生物学途径。采用 CellMiner 数据库和分子对接来识别 ABI3 蛋白和特定抗癌剂之间的潜在相互作用。研究结果：ABI3 表达及其预测预后的能力因不同肿瘤而异，在 Tprolif 细胞和单核细胞/巨噬细胞中观察到特别高的表达。在大多数恶性肿瘤中，拷贝数变异 (CNV) 和甲基化与 ABI3 表达呈负相关。相应的突变生存分析表明，ABI3的突变状态与LGG患者的预后密切相关。 ABI3 表达与免疫治疗生物标志物和癌症反应相关。估计和免疫浸润分析表明 ABI3 与免疫抑制相关。 ABI3 与免疫调节因子和免疫相关通路显着相关。最后，筛选出潜在的 ABI3 靶向药物并与 ABI3 蛋白对接。解释：我们的研究表明 ABI3 是一种强大的肿瘤生物标志物。其功能至关重要，可以抑制肿瘤细胞的异位转移并调节细胞粘附和迁移。这里介绍的发现可能会对新的抗癌抑制剂的产生产生显着的影响，特别是那些针对 BRCA 的抑制剂。版权所有 © 2023 Sun, Cai, Xiong, Xie, Li, Xie, Luo, Hu,zhong 和 Wang。

Background: Abelson interactor Family Member 3 (ABI3) encodes protein that not only suppresses the ectopic metastasis of tumor cells but also hinders their migration. Although ABI3 had been found to modulate the advancement of diverse neoplasms, there is no comprehensive pan-cancer analysis of its effects. Methods: The transcriptomics data of neoplasm and normal tissues were retrieved from the Genomic Data Commons (GDC) data portal, and UCSC XENA database. To gather protein information for ABI3, Human Protein Atlas (HPA) and GeneMANIA websites were utilized. Additionally, Tumor Immune Single-cell Hub (TISCH) database was consulted to determine the primary cell types expressing ABI3 in cancer microenvironments. Univariate Cox regression approach was leveraged to evaluate ABI3's prognostic role across cancers. The Cbioportal and Gene Set Cancer Analysis (GSCA) website were leveraged to scrutinize the genomic landscape information across cancers. TIMER2.0 was leveraged to probe the immune cell infiltrations associated with ABI3 across cancers. The associations of ABI3 with immune-related genes were analyzed through Spearman correlation method. Gene Set Enrichment Analysis (GSEA) and Gene Set Variation Analysis (GSVA) were utilized to search associated biological pathways. The CellMiner database and molecular docking were implemented to identify potential interactions between the ABI3 protein and specific anticarcinogen. Findings: ABI3 expression and its ability to predict prognosis varied distinct tumor, with particularly high expression observed in Tprolif cells and monocytes/macrophages. Copy number variation (CNV) and methylation negatively correlated with ABI3 expression in the majority of malignancies. Corresponding mutation survival analysis indicated that the mutation status of ABI3 was strongly connected to the prognosis of LGG patients. ABI3 expression was linked to immunotherapeutic biomarkers and response in cancers. ESTIMATE and immune infiltrations analyses presented ABI3 association with immunosuppression. ABI3 was significantly correlated with immunoregulators and immune-related pathways. Lastly, prospective ABI3-targeted drugs were filtered and docked to ABI3 protein. Interpretation: Our study reveals that ABI3 acts as a robust tumor biomarker. Its functions are vital that could inhibit ectopic metastasis of tumor cells and modulate cellular adhesion and migration. The discoveries presented here may have noteworthy consequences for the creation of fresh anticancer suppressors, especially those targeting BRCA.Copyright © 2023 Sun, Cai, Xiong, Xie, Li, Xie, Luo, Hu, Zhong and Wang.