EHD1 (EH Domain Containing 1)

Notably, these include the Wnt/β-catenin axis. Candidate biomarkers with potential prognostic and therapeutic relevance in diabetic breast cancer (BC) were also identified.

Importantly, celecoxib, an U.S. Food and Drug Administration (FDA)-approved drug, inhibits O-GlcNAcylation and exerts antitumor effects. These findings reveal a pathological role for cytokine O-GlcNAcylation in LUAD and identify this axis as a potential therapeutic target.

Collectively, our findings provide robust molecular evidence that CC and RC follow divergent oncogenic pathways, emphasizing the need for site-specific biomarker development and therapeutic targeting in colorectal cancer.

Our study illuminates the role of m6A-modified EHD1 in tumor immune evasion and immunotherapy responses, thereby offering a novel avenue to potentially enhance immunotherapeutic sensitivity and improve the prognosis for patients with LUAD.

These findings collectively suggest that phagocytic uptake of EBV-infected lymphocytes or their components may serve as a primary infection mechanism for ECs, potentially establishing an immunosuppressive microenvironment that contributes to tumor progression and poor clinical outcomes, though the exact molecular pathways require further elucidation.IMPORTANCEClinical investigations of NPC specimens identified EBERs-positive endothelial cells as clinically significant biomarkers, demonstrating robust correlations with lymphatic metastasis (P < 0.05), distant metastasis (P < 0.01), and advanced tumor staging (P < 0.01), while immunological profiling of affected patients revealed concomitant reductions in B-cell populations (P < 0.01), collectively indicative of systemic immunoregulatory status. Furthermore, integrative experimental approaches incorporating live-cell dynamic imaging, single-cell transcriptional profiling, and ultrastructural electron microscopy provided compelling evidence that endothelial phagocytosis of lymphocytes serves as a principal route for EBV cellular entry and subsequent modulation of the NPC tumor microenvironment.

Remarkably, EHD1 can activate the AKT-mTOR pathway to upregulate the protein expression of hypoxia-inducible factor 2α (HIF2α) under normoxic conditions and subsequently enhance the invasive and metastatic breast cancer. Our findings indicated EHD1 as a new regulator of HIF2α and a potential therapeutic target for inhibiting breast cancer metastasis.

In the current study, the authors describe a new functional link between the NEKLs and several proteins with known roles in endocytosis including TAT-1, a conserved enzyme that moves lipids between the bilayers of cellular membranes. As previous work implicated NEKLs in developmental defects and cancer, the present study can provide new insights into how the misregulation of endocytosis affects human health and disease.

As the key of ceRNA regulatory network, the expression of miRNA-21-5p in lung cancer patients was significantly higher than that in healthy people (P < 0.01), and its high expression was significantly associated with poor prognosis (P = 0.0025). Our study successfully constructed a MIR99AHG-hsa-miR-21-5p-EHD1 mutually regulatory network, suggesting the potential efficient biomarkers in LC.

High plasma levels of a 9-gene signature (BECN1, PRKCB, COPA, TSC22D3, MAP2K3, UQCRHL, PTMAP4, EHD1, NAP1L1 pseudogene) and a 5-gene signature (FTH1P7, PTMAP4, ATF4, FTH1P8, ARMC7) were significantly associated with inferior progression-free and overall survival in DLBCL patients, respectively, independent of the NCCN-IPI score. Total RNA sequencing of blood plasma samples allows the analysis of the cell-free transcriptome in DLBCL and PMBCL patients and demonstrates its unexplored potential in identifying diagnostic, cell-of-origin, and prognostic cfRNA biomarkers.

Our pilot study concluded that thyroidal EHD1 expression is a biomarker for DTC in adults. EHD1 expression was not associated with DTC aggressiveness in cases without metastatic disease – this needs further investigation in metastatic DTC to identify a prognostic role of EHD1.

Conversely, EHD1 overexpression-dependent exaggerated oncogenic traits require IGF-1R expression and kinase activity. Our findings define the RTK traffic regulation as a proximal mechanism of EHD1 overexpression-dependent oncogenesis that impinges on IGF-1R in EWS, supporting the potential of IGF-1R and EHD1 co-targeting.

Furthermore, the suppression of SFPQ could inhibit hyper-malignant phenotype HCC cells, while the WB results showed that inhibition of SFPQ expression also resulted in lower expression of necroptosis proteins, compared to the sh-NC group. Our prognostic model could accurately predict the prognosis of patients with HCC to further identify novel molecular candidates and interventions that can be used as alternative methods of treatment for HCC.