ESM1 (Endothelial Cell Specific Molecule 1)

Taken together, our study shows that PRDM1 silencing promotes ferroptosis and sunitinib sensitivity by inhibiting ESM1 transcription and modulating PI3K/Akt signaling in RCC. Our findings thus provide novel insights for therapeutically targeting RCC.

In OC mice, TRIM28 overexpression promotes angiogenesis and Bev resistance via ESM1-mediated ITGB1/FAK activation. This work unveils a new molecular pathway underlying Bev resistance in OC and proposes TRIM28 and ESM1 as potential therapeutic targets.

Diff-Metabolic cells retained liver-specific functions with favorable prognosis, whereas the other three programs correlated with disease advancement; notably, all four states exhibited differential therapeutic vulnerabilities, including sorafenib resistance...Geneformer-based virtual knockout screening identified HSP90B1 as a convergent dependency, validated by its cancer cell essentiality, HCC overexpression, abundance in treatment-resistant tumors, and association with adverse survival. This integrated atlas establishes a framework for targeting tumor-intrinsic states and microenvironmental dependencies in HCC.

Human umbilical vein endothelial cells (HUVECs) were treated with varying concentrations of Ang II, endocan, tumor necrosis factor-α (TNF-α), or endocan with or without TNF-α inhibitor, etanercept, followed by analysis of phosphorylated eNOS (Ser1177) via western blot and nitrite levels via Griess assay...Notably, TNF-α inhibition reversed endocan-induced reductions in eNOS phosphorylation and nitrite levels. Our findings reveal a novel pathogenic mechanism whereby endocan drives endothelial dysfunction and hypertension through TNF-α-mediated eNOS suppression, establishing endocan as a promising therapeutic target for cardiovascular disease.

Overexpressed ESM1 may mediate a reduced level of immune cell infiltration in TME through immune signalling pathways. ESM1 can be used as a predictive biomarker for immune-related and clinical progression in BC.

FP attenuates colonic injury and intestinal inflammatory response in CRC mice, repairs disrupted-intestinal microbiota, and improves metabolites. This research provides experimental basis for application of FP as a potential therapeutic agent for CRC.

When administered either alone or in combination with a biologic disease-modifying antirheumatic drug, etanercept, ESMA04 demonstrated therapeutic efficacy in CIA mice. Overall, our findings identified SNORD3-EZH2-ESM1 signaling as a driver of RA-FLS pathogenesis and underscored the promise of aptamer-based therapies for RA treatment.

Quantitative analysis of coronary thrombus components revealed significant positive correlations between sCD40-L, hs-CRP, VCAM-1 levels and CMVO prevalence. Moreover, systemic metabolic disturbances - particularly type 2 diabetes mellitus, elevated serum LDL-C concentrations and heightened IL-6 levels were identified as independent predisposing factors for CMVO development.

Our study demonstrates that HOXD4-mediated transcriptional activation of ESM1 enhances GBM cell malignant phenotypes and tumor angiogenesis in GBM.

Furthermore, based on the SERPINH1-related differentially expressed genes, a prognostic risk model was constructed, successfully identifying PLOD1, ITGA5, and ESM1 as core collaborative genes affecting patient prognosis. Overall, our findings underscore the multiple functions of SERPINH1 as a hub for cervical cancer metastasis regulation, suggesting its potential as a promising biomarker for tailoring strategies in metastasis patients of CESC.