Fam83a, Family with sequence similarity 83 member A, has emerged as an oncogene involved in multiple signaling pathways. It is closely associated with the Wnt/β -catenin pathway, and also has links to other processes like autophagy, epithelial-mesenchymal transition (EMT), and cell proliferation and migration. Its dysregulation has significance in various cancers, highlighting its importance in tumorigenesis [1,2,4-10].

In pancreatic cancer, Fam83a binds directly to β -catenin, inhibiting the cytoplasmic destruction complex, phosphorylation, and degradation of β -catenin. Phosphorylation at tyrosine 138 by BLK enhances Wnt/β -catenin-mediated transcription, promoting pancreatic tumorigenesis [1]. In ovarian cancer, inhibiting Fam83a suppresses cell proliferation, invasion, and enhances chemosensitivity, while its upregulation has opposite effects, acting through the Akt/Wnt/β -catenin pathway [2]. In head-neck squamous cell carcinoma (HNSCC), Fam83a promotes cell growth, metastasis, and EMT via activating the Wnt/β -catenin signaling pathway [3].

In conclusion, Fam83a plays crucial oncogenic roles mainly through its interactions with the Wnt/β -catenin pathway in cancers such as pancreatic, ovarian, and HNSCC. These findings from in-vitro and in-vivo studies provide insights into its function in tumorigenesis, suggesting that targeting Fam83a could potentially be a therapeutic strategy for these cancer types.