A pan-cancer analysis of the oncogenic role of branched-chain aminotransferase 1 (BCAT1) in human tumors
TL;DR
BCAT1 expression was significantly upregulated in most malignancies, and high expression was associated with worse OS and DFS in multiple cancer types, highlighting its potential as a pan-cancer biomarker and therapeutic target.
Abstract
Based on emerging evidence implicating branched-chain aminotransferase 1 (BCAT1) in tumorigenesis from animal and cellular studies, this study aimed to systematically evaluate its oncogenic role through a pan-cancer analysis to address the lack of comprehensive pan-cancer investigations in the literature. Using datasets from The Cancer Genome Atlas and the Genotype-Tissue Expression project, we analyzed BCAT1 expression, prognosis, genetic alterations, immune infiltration, and functional enrichment across 33 cancer types. The primary endpoints were overall survival (OS) and disease-free survival (DFS). Statistical significance was primarily defined as P < .05. For analyses involving multiple correlations across cancer and immune cell types, the false discovery rate < 0.05 was applied. BCAT1 was significantly upregulated in most malignancies, and high expression was associated with worse OS and DFS in multiple cancer types. BCAT1 expression correlated with reduced CD8+ T cell infiltration and increased cancer-associated fibroblast accumulation across several tumors. Enrichment analyses suggested BCAT1 involvement in RNA metabolism and intracellular protein processing. BCAT1 was significantly upregulated in most malignancies, and high expression was associated with worse OS and DFS in multiple cancer types, including adrenocortical carcinoma (hazard ratio = 6.3) and lower-grade glioma (hazard ratio = 2.6) (all log-rank P < .05), highlighting its potential as a pan-cancer biomarker and therapeutic target. The present findings are associative and require further experimental and external validation.