LGALS1 (Galectin 1)

The upregulated LGALS1 is then secreted via SUSD2 assistance, ultimately suppressing CD8+ T cell function and inducing apoptosis. Our findings define a stromal-immune axis in pancreatic cancer, linking miR-181b-5p from CAFs to the establishment of an immune-suppressive niche via the STING pathway in tumor cells, thereby revealing this cascade as a targetable mechanism to counteract immune evasion.

By integrating germline (GWAS-based) and somatic evidence, this study provides a comprehensive view of HCC pathogenesis. This integrated strategy successfully identified a core set of genes and proteins with potential causal links to HCC, elucidating their functional convergence in cancer biology. These findings offer novel molecular insights and candidate targets for precise diagnosis, prognostic assessment, and targeted therapy of HCC, laying a solid foundation for future translational research.

This study represents the first to systematically elucidate that galectin-1 expression in GC tissues and peritoneal fibrosis are independent predictors of the risk of PM in patients with GC. These two indicators coordinate with pT stage, and the combination of these two indicators increases their predictive accuracy.

In contrast, SiHa spheroids represented selective responses: MSC-exosome pretreatment did not enhance sensitivity to paclitaxel-cisplatin but improved responsiveness to paclitaxel-carboplatin, particularly within the spheroid core. Overall, MSC-exosome pretreatment exerts cell type and drug-specific effects in CC spheroids, supporting their potential to modulate chemotherapy response.

We systematically characterize the stage-specific functional shifts of Gal-1 in liver disease: it serves as a double-edged immunomodulator during hepatitis, acts as a core driver of fibrosis progression, and ultimately functions as a multifunctional pro-tumorigenic factor in established HCC. This "glyco-code interpreter" model offers a new perspective on the complexities of chronic hepatic injury and may provide a theoretical basis for developing novel therapeutic strategies that target this key regulatory framework.

This study demonstrated a novel role of LGALS1 in mature osteoblast-like cells. Further investigation into the regulatory pathways is warranted.

The gap between pre‑clinical findings and clinical applications highlights the need for further investigation. Extensive research is still required to elucidate how therapeutic interventions achieve efficacy, ensure safety, and identify optimal strategies for targeting different organs in combination with other pharmacological agents.

Their primary structural feature is the modification of a thiodigalactoside scaffold at the 3- and 3'-positions with a half-sandwich ruthenium(II) arene complex containing a bidentate 4-(2-pyridyl)-1H-1,2,3-triazol-1-yl ligand. The most potent inhibitor in the series efficiently blocked the binding of hGal-1 to the surface of MDA-MB-231 tumor cells, reduced their viability, and completely suppressed hGal-1-induced phosphatidylserine exposure in Jurkat cells, a process previously described as preaparesis rather than classical apoptosis.

Targeting mTOR signaling contributes to the regulation of Galectin-1 immune checkpoint activity in KMT2Ar-ALL. Inhibition of mTOR may represent a potential therapeutic strategy to overcome immune evasion in this leukemia subtype.

Our findings unveil a novel phosphorylation-dependent DUSP22-LGALS1 axis that reprograms the immunosuppressive TME. This work thus proposes a promising therapeutic strategy to overcome immune checkpoint blockade resistance in breast cancer.

The integration of these biomarkers with superior atrial imaging enables a broader understanding of the fibrotic substrate of atrial fibrillation. This combined molecular imaging approach can facilitate risk stratification, refine therapeutic decisions, and facilitate early identification of higher-risk metabolic phenotypes, thus potentially facilitating directed antifibrotic and anti-inflammatory therapy in atrial fibrillation.

Our findings provide new insights into the metabolic and immunological mechanisms underlying SOC, and highlight potential targets for therapeutic interventions.