Investigation of the function of the novel tumor marker BEND5 in lung adenocarcinoma based on data mining and in vitro analysis

BEN domain-containing protein 5 (BEND5) belongs to the BEN family of structural domains, whose members can be found in several animal proteins. The characteristic ability of BEND5 to inhibit cell proliferation allows it to play a crucial role as a tumor suppressor gene in colorectal cancer. However, the function of BEND5 in lung adenocarcinoma (LUAD) has not been fully explored.

BEND5 expression is low in LUAD and may be associated with poor prognosis, and BEND5 overexpression inhibits LUAD cells via the PPAR signaling pathway. The dysregulation of BEND5 in LUAD, its prognostic significance, and its ability to function in vitro suggest that BEND5 could be a deciding factor in the progression of LUAD.

The Cancer Genome Atlas (TCGA) database was used to extensively examine BEND5 dysregulation and its prognostic significance in pan-cancer data. Databases including TCGA, gene expression profiling interactive analysis (GEPIA), and STRING were used to perform analysis of the expression pattern and clinical significance of BEND5 in patients with LUAD, and the possible regulatory mechanisms responsible for the occurrence and progression of LUAD. To explore the relationship between BEND5 expression and tumor immunity in LUAD. Finally, transfection experiments using an in vitro model were performed to confirm BEND5 expression in LUAD cells while investigating its regulatory significance in tumor cell proliferation.

Significantly decreased BEND5 expression was observed in LUAD and in most other cancers. Further analysis of the Kyoto Encyclopedia of Genes and Genomes database revealed that the genes significantly linked to BEND5 were mainly enriched in the peroxisome proliferator-activated receptor (PPAR) signaling pathway. Also, BEND5 was found to be involved in tumor immunity in LUAD via its functional regulation of various tumor cell types, such as B cells and T cells. In vitro experimental results showed that BEND5 overexpression mediated LUAD cell inhibition and decreased the expression of cell cycle-related proteins. Further, BEND5 activated the PPAR signaling pathway, and knockdown of PPAR reversed the effect of BEND5 overexpression on LUAD cells. Conclusions: BEND5 expression is low in LUAD and may be associated with poor prognosis, and BEND5 overexpression inhibits LUAD cells via the PPAR signaling pathway. The dysregulation of BEND5 in LUAD, its prognostic significance, and its ability to function in vitro suggest that BEND5 could be a deciding factor in the progression of LUAD.