ETS1 (ETS Proto-Oncogene 1)

Together, these findings suggest that PRAME and ETS2 cooperatively suppress ciliogenesis in melanoma cells, proposing a previously unrecognized epigenetic mechanism of ciliary loss. This mechanism broadens our understanding of melanoma progression and highlights the role of the PRAME-ETS2-HDAC1 axis in regulating ciliogenesis.

The identification and validation of biomarkers reflecting this continuum could enable the establishment of molecular margins-improving risk assessment, reducing local recurrence, and advancing personalized oncologic surgery in HNSCC. Standardizing definitions and sampling protocols for "normal adjacent tissue" remains essential for future translational research.

ETS-family proteins from all major classes bind CPD-containing DNA sites.Engagement of CPD by ETS proteins inhibits DNA repair in a position-dependent manner.Structure and thermodynamics of ETS binding to damaged DNA differ from undamaged substrates.

These results demonstrate that cNOS regulates IKKα at multiple levels-promoter activation, transcriptional elongation, and protein stability. This multilayered control enhances our understanding of UV-induced skin pathogenesis and supports cNOS-IKKα signaling as a potential target for therapeutic intervention in skin cancer.

Furthermore, we identified ETS proto-oncogene 1 (ETS1) as a transcriptional activator of ZBP1 under HG conditions. In summary, this study identifies ZBP1 as a key mediator of tubular injury, inflammation and fibrosis in DN via RIPK3-dependent necroptosis, highlighting its potential as a therapeutic target.

Further investigation demonstrated that miR-338-3p exerts its tumour-suppressive effects by directly targeting ETS1, and the hsa_circ_0000977/miR-338-3p/ETS1 axis regulates the proliferation and migration of CCA cells. We have concluded that hsa_circ_0000977 drives CCA progression by sponging miR-338-3p and modulating its target ETS1, suggesting its clinical value for predicting outcomes and developing targeted therapies.

These genes demonstrated substantial discriminatory capability, with an area under the curve ranging from 0.95 to 0.99, and were found to be functionally linked to immune system dysfunction, cytokine signaling, NF-κB activation, and a maladaptive stress response. These findings link MRONJ to systemic immune-inflammatory imbalance and translational stress disruption, offering novel insights and potential biomarkers for diagnosis and risk evaluation.

Moreover, the combination of dasatinib with an anti-programmed cell death protein-1 (PD-1) antibody represents a potential therapeutic strategy. These findings highlight dasatinib as a potential therapeutic option for metastatic TNBC and suggest that selecting patients with high ETS1 expression may optimize treatment response.

M2 macrophage-derived exosomal miR-668-3p promotes DDP resistance in GC cells by targeting the ETS1/EGFR axis, thereby activating the autophagy pathway. Future research should focus on developing targeted inhibition strategies for miR-668-3p to effectively reverse DDP resistance in GC cells, optimizing its potential for clinical application.

To functionally validate this finding, we employed lipid nanoparticle (LNP)-mediated co-delivery of si-circPPFIA2 and enzalutamide, which effectively restored drug sensitivity and inhibited tumor growth in resistant PCa models. Our findings highlight circPPFIA2 as both a prognostic biomarker and a promising therapeutic target for advanced PCa, providing a rationale for developing circRNA-directed therapies to overcome treatment resistance.

The prognostic relevance of VEGF-A in LSCC is region-dependent, with clinically meaningful value confined to tumor depth. Together with a high-risk three-miRNA signature, these findings delineate two molecular subgroups capturing most recurrences and may inform sampling strategies and risk stratification.

The Editor apologizes to the readership of the Journal for any inconvenience caused. [International Journal of Molecular Medicine 44: 593‑607, 2019; DOI: 10.3892/ijmm.2019.4206].