FAXC, a gene with currently no known common aliases, has been implicated in multiple biological processes. In mammals, its function was previously unknown, but recent research shows it may play roles in tumorigenesis and muscle development. It could be involved in pathways related to epithelial-mesenchymal transition, hypoxia, and KRAS signaling based on transcriptome data, and is potentially crucial for understanding the regulatory mechanisms of muscle development [1,2].

In cholangiocarcinoma (CCA) research, knockdown of FAXC in mice reduced subcutaneous tumorigenicity. FAXC binds to tumor-promoting genes ANXA2 and c-SRC, forming a complex in the mitochondria. FAXC enhances SRC-dependent ANXA2 phosphorylation at tyrosine-24, with its C-terminal amino acid residues (351-375) required for this phosphorylation [1].

In buffalo myoblasts, the enhancer Enh483, which has a direct association with the FAXC promoter, regulates myoblast proliferation and differentiation. Inhibition of Enh483 led to decreased expression of myogenic proliferation and differentiation marker genes [2].

In summary, FAXC is involved in tumorigenesis in cholangiocarcinoma and muscle development in buffalo. The knockdown experiments in mice for CCA and the manipulation of enhancer-FAXC interaction in buffalo myoblasts have revealed these functions. Understanding FAXC's role can potentially provide new therapeutic targets for cholangiocarcinoma and contribute to the improvement of meat-related traits in buffalo through better understanding of muscle development [1,2].