FUCA2, or 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 in oligosaccharide chains, which contributes to various biological processes. Aberrant fucosylation related to FUCA2 has implications in disease development, including its role in cell-extracellular matrix interactions and cell signaling pathways [5].

In cancer research, FUCA2 shows upregulation in most tumors and is associated with poor survival rates. Knockdown of FUCA2 in lung cancer cells inhibited cell viability, indicating its potential oncogene role [1]. In triple-negative breast cancer (TNBC), cancer-associated adipocytes secrete FUCA2, which promotes TNBC growth and metastasis through interaction with TM9SF3 [2]. In gastric cancer, FUCA2 expression was markedly increased in tumor tissues compared with non-tumoral tissues and was associated with advanced surgical staging and histological grade [3]. In hepatocellular carcinoma, increased FUCA2 expression is related to age, overall survival, and immune infiltration [4]. In lung adenocarcinoma, FUCA2 upregulates GGH to modulate cell cycle and epithelial-mesenchymal transition, promoting tumor progression [6].

In conclusion, FUCA2 is closely associated with cancer progression, with its upregulation often linked to poor prognosis in multiple cancer types. The findings from in vitro cell-based knockdown experiments and in vivo studies in cancer models have revealed its oncogenic role, highlighting its potential as a therapeutic target in cancer treatment.