FUCA2, also known as alpha-L-fucosidase 2, is a member of the glycoside hydrolase (GH) families 29A. It is involved in the hydrolysis of terminal L-fucose residues linked to the reducing end of N-acetyl glucosamine (GlcNAc) of oligosaccharide chains, which is related to the defucosylation process influencing various biological processes and disease developments [5].

In cancer research, FUCA2 has emerged as a significant gene. It is upregulated in most tumors and is associated with poor survival rates. For example, in lung cancer cells, knockdown of FUCA2 inhibits cell viability, indicating its oncogene role [1]. In triple-negative breast cancer (TNBC), cancer-associated adipocytes secrete FUCA2 to promote TNBC growth and metastasis through interaction with TM9SF3 [2]. In gastric cancer, FUCA2 expression is markedly increased and is associated with advanced surgical staging and histological grade [3]. In hepatocellular carcinoma, increased FUCA2 expression is related to a poor prognosis and immune infiltration [4]. In lung adenocarcinoma, the FUCA2/GGH axis promotes tumor progression by regulating the cell cycle and epithelial-mesenchymal transition [6].

In conclusion, FUCA2 is mainly associated with cancer progression and prognosis. Its over-expression in various cancers, as revealed by knockdown experiments in cancer cell lines, indicates its oncogenic function. These findings contribute to understanding the role of FUCA2 in cancer development and may provide potential targets for tumor therapy.