The TCP transcription factor family is a plant-specific group of regulators with well-documented roles in mediating abiotic stress responses. Licorice (Glycyrrhiza) is a high-value medicinal crop of global economic significance, predominantly cultivated in arid and semi-arid environments where saline soils constrain seed germination, impair seedling development, and diminish both rhizome biomass and the accumulation of pharmacologically active metabolites. Despite the agronomic importance of this genus, a systematic genome-wide survey of the TCP family and its contribution to salt tolerance in Glycyrrhiza has not been reported. Here, we identified members of the TCP gene family at the whole-genome level in three representative species—G. uralensis, G. inflata, and G. glabra—and performed integrated bioinformatic characterization encompassing phylogenetic classification, chromosomal distribution, conserved motif architecture, physicochemical parameters, cis-regulatory element composition, and synteny analysis. Transcriptomic profiling revealed that Glycyrrhiza TCP genes display pronounced tissue-specific expression and undergo dynamic transcriptional reprogramming under saline conditions. Among the salt-responsive candidates, GuTCP16 emerged as a key regulator; it was confirmed to localize to the nucleus, and its heterologous expression in Arabidopsis enhanced plant performance under salt stress, demonstrating that GuTCP16 acts as a positive modulator of salt tolerance. Taken together, this work delineates the evolutionary features and functional diversification of the TCP family in Glycyrrhiza and identifies candidate genes to support molecular breeding efforts aimed at developing salt-resilient licorice cultivars.

Metabolic reprogramming is closely linked to tumor proliferation, invasion, and immune escape. Despite its central role in amino acid metabolism, the regulatory mechanisms of asparagine metabolism in hepatocellular carcinoma (HCC) progression remain poorly characterized. Rather than focusing on canonical metabolic genes, prognostic markers were identified from co-expression modules associated with asparagine metabolism signatures. Using the TCGA database and asparagine metabolism-related gene sets, a prognostic risk-scoring model was developed through differential expression analysis, univariate Cox regression, and the LASSO algorithm and externally validated with the GEO dataset (GSE14620). Survival analysis, ROC curve evaluation, nomogram construction, scRNA-seq, GSEA, and drug sensitivity analysis were performed to systematically delineate the molecular mechanisms by which asparagine metabolism drives HCC progression. A three-gene signature comprising BOP1, SAC3D1, and PDE2A effectively stratified patients into high- and low-risk groups. High-risk patients exhibited markedly poorer overall survival, enrichment in tumor proliferation-associated pathways, increased tumor purity, reduced immune cell infiltration, and a substantially higher TP53 mutation rate (38% vs. 13%). In contrast, the low-risk group showed enrichment in pathways linked to hepatoblastoma suppression and liver function, alongside improved predicted response to immunotherapy. Single-cell analysis identified NK cells and endothelial cells as central mediators of asparagine metabolism-driven HCC progression, with BOP1, SAC3D1, and PDE2A displaying dynamic expression patterns during differentiation. Furthermore, the high-risk group was predicted to be more sensitive to chemotherapeutics such as cyclophosphamide and 5-fluorouracil. These findings highlight a potential interplay between nitrogen metabolism and asparagine metabolism in HCC and suggest mechanisms by which these pathways may influence NK cell and endothelial cell function to promote disease progression. This study establishes a novel prognostic model and identifies potential chemotherapeutic vulnerabilities in high-risk patients, warranting further experimental and clinical validation.