PTGR1 (Prostaglandin Reductase 1)

This risk score showed a significant correlation with glucose metabolism and reflected immune cell infiltration patterns. The core model gene, CCL20, promotes HCC cell proliferation and migration, supporting its potential as a valuable prognostic biomarker and a therapeutic target for HCC.

These findings provide the first evidence of the NLRP3 inflammasome/pyroptosis pathway's involvement in MAFLD-associated HCC development. The data strongly suggest that metabolic dysregulation and NLRP3-driven inflammation lead to pyroptosis, triggering ongoing cycles of cellular damage and regeneration and accelerating the transition from MAFLD to HCC.

The FAM-related gene signature developed in this study provides a reliable tool for predicting poor outcomes in glioma patients. PTGR1, identified as a pivotal gene within this signature, may serve as a potential target for future therapeutic interventions, offering promising avenues for enhancing patient survival.

Covalent docking, informed by prior chemoproteomic cross-linking data, revealed a highly favorable binding pose for licochalcone A at the NADPH-binding site. This pose aligned with a transient noncovalent binding pose inferred from solvent site-guided molecular docking, emphasizing the stereochemical complementarity of the coenzyme-binding site to licochalcone A. Sequence analysis across PTGR1 orthologs in vertebrates and exploration of 3D structures of human NADPH-binding proteins further underscore the potential of the coenzyme-binding site as a scaffold for developing PTGR1-specific inhibitors, positioning licochalcone A as a promising lead compound.

Additionally, increased E2F4 levels facilitated PTGR1 transcription by directly binding to the PTGR1 promoter. This study demonstrated the oncogenic properties of NUCB2 in HCC and suggested that NUCB2 facilitates hepatocellular carcinoma progression by activating the E2F4/PTGR1 axis.

P4, N=70, Not yet recruiting, Shanghai Sixth People's Hospital; Shanghai Sixth People's Hospital

Next, through co-culture experiments, we simulated the tumor microenvironment and used immunohistochemistry staining to observe and analyze the distribution and activation status of M2 macrophages and CD8+ T cells in the co-culture system. We validated in vivo experiments the molecular mechanism by which the target gene regulates immune cell impact on TNBC progression.

Therefore, they might have tumor suppressor activity in GC progression. New potential biomarkers and pathways involved in GC and IM were identified that are important for the transformation of GC from IM to adenocarcinoma and can be therapeutic targets for GC.

These preclinical findings illustrate the potential of LP-184 as a pan-HRD cancer therapeutic. Taken together, our results support continued clinical evaluation of LP-184 in a large subset of HRD solid tumors.

Of note, DHCR24 is a key enzyme involved in cholesterol biosynthesis, and its overexpression promotes the proliferation and migration of LSCC cells. These findings suggest that DHCR24 is a novel molecule associated with FSCN1 in LSCC, and that the FSCN1‑DHCR24 interaction may promote LSCC progression by regulating cholesterol metabolism‑related signaling pathways.

Furthermore, cell-cycle arrest occurred in the G1 phase by suppressing Cyclin D1. In summary, 6-GPS may play a crucial role in the occurrence and development of OSCC and has the potential to be developed further as a diagnostic, therapeutic, and prognostic tool for OSCC.