WIF1（Wnt抑制因子1）是一种强效的肿瘤抑制基因，在许多恶性肿瘤中表观遗传学上被沉默。尽管它们参与了几种恶性肿瘤的下调，但WIF1蛋白与Wnt通路分子的关联尚未得到充分探索。本研究采用表达、基因本体分析和通路分析相结合的计算方法，以了解WIF1蛋白的作用。此外，我们通过Wnt通路分子与WIF1领域的交互来确定其抑制肿瘤的作用，同时确定它们的可能相互作用。初步的蛋白质相互作用网络分析赋予了我们Wnt配体（如Wnt1、Wnt3a、Wnt4、Wnt5a、Wnt8a和Wnt9a）、Frizzled受体（Fzd1和Fzd2）和低密度脂蛋白复合物（Lrp5/6）作为蛋白的最重要的相互作用因素。进一步，我们使用癌症基因图谱来确定上述基因和蛋白的表达分析，以了解这些信号分子在主要癌症亚型中的重要性。此外，使用分子对接研究探索上述大分子实体与WIF1领域的关联，而使用100ns的分子动力学模拟研究它们的动力学和稳定性。因此，我们了解到WIF1在抑制各种恶性肿瘤中的Wnt通路中扮演着可能的角色。由Ramaswamy H.Sarma传达。

WIF1 (Wnt inhibitory factor 1) is a potent tumour suppressor gene which is epigenetically silenced in numerous malignancies. The associations of WIF1 protein with the Wnt pathway molecules have not been fully explored, despite their involvement in the downregulation of several malignancies. In the present study, a computational approach encompassing the expression, gene ontology analysis and pathway analysis is employed to obtain an insight into the role of the WIF1 protein. Moreover, the interaction of the WIF1 domain with the Wnt pathway molecules was carried out to ascertain the tumour-suppressive role of the domain, along with the determination of their plausible interactions. Initially, the protein-protein interaction network analysis endowed us with the Wnt ligands (such as Wnt1, Wnt3a, Wnt4, Wnt5a, Wnt8a and Wnt9a), along with the Frizzled receptors (Fzd1 and Fzd2) and the low-density lipoprotein complex (Lrp5/6) as the foremost interactors of the protein. Further, the expression analysis of the aforementioned genes and proteins was determined using The Cancer Genome Atlas to comprehend the significance of the signalling molecules in the major cancer subtypes. Moreover, the associations of the aforementioned macromolecular entities with the WIF1 domain were explored using the molecular docking studies, whereas the dynamics and stability of the assemblage were investigated using 100 ns molecular dynamics simulations. Therefore, providing us insights into the plausible roles of WIF1 in inhibiting the Wnt pathways in various malignancies.Communicated by Ramaswamy H. Sarma.