BEND5, belonging to the BEN family of structural domains, has been identified as a crucial gene in multiple biological contexts. It functions as a tumor suppressor gene, inhibiting cell proliferation. It is involved in pathways such as the Notch signaling pathway and the peroxisome proliferator-activated receptor (PPAR) signaling pathway, playing a significant role in cancer development and other biological processes [1,2].

In breast cancer, low BEND5 expression predicts advanced stage and shorter overall survival. Functional experiments show that BEND5 suppresses breast cancer growth and metastasis in vitro and in vivo by inhibiting Notch signaling. It directly interacts with transcription factor RBPJ/CSL, preventing the formation of a transcription activation complex with MAML [1].

In lung adenocarcinoma, BEND5 expression is low, associated with poor prognosis, and overexpression inhibits cells via the PPAR signaling pathway [2].

In colorectal cancer, hypermethylation of BEND5 contributes to cell proliferation, and its expression is downregulated. BEND5 hypermethylation is associated with poor overall survival, and the gene functions as a prognostic marker [3].

In conclusion, BEND5 functions as a tumor suppressor gene, inhibiting cell proliferation in breast, lung, and colorectal cancers. Its involvement in key signaling pathways provides potential therapeutic targets. The study of BEND5 in these cancer models helps in understanding the disease mechanisms and may offer new strategies for cancer treatment.