NPY1R (Neuropeptide Y Receptor Y1)

Here, we show that seizure causing meningiomas demonstrate distinct clinical, radiographic, chromosomal, and transcriptional features. Novel associations with seizure presentation in meningioma include MenG C status, chromosome 14q loss, and seizure-specific dysregulation of neurotransmitter receptor genes.

Furthermore, we identified miR-141 as a negative regulator of NPY1R, highlighting its potential as a therapeutic agent. Collectively, our results identified the UHRF1/NPY1R regulatory axis as a critical epigenetic mechanism in intestinal inflammation and underscored its dual promise for IBD diagnostics and therapy.

Moreover, 211At-ATE-KINW had better tumor growth inhibition and significantly prolonged survival in U87-MG cell xenograft models compared to free 211At. Thus, a novel specific NPY1R peptide has potential to be applied in development of 68Ga/ 211At-labeled radiopharmaceuticals for glioma-targeted imaging and therapy.

Knockdown of ERα/ERβ exacerbated, while their overexpression rescued, the lipid-metabolic disruption induced by PFOA/PFOS. These findings indicate that EDCs such as PFOA and PFOS may promote HCC progression by disrupting lipid metabolism via interference with NR-dependent gene regulation, highlighting a novel environmental-toxicological axis in hepatocarcinogenesis.

This study, through the integration of multi-omics data, establishes EMP1 as a reliable marker of activated HSCs. The genes NPY1R, CTHRC1, IGFBP3, and ADH1B play critical regulatory roles and exhibit prognostic value in the progression from hepatic fibrosis to HCC. Our findings provide novel insights and therapeutic targets for the use of Salvia miltiorrhiza in treating hepatic fibrosis and HCC.

We identify NPY-NPY1R-TGFβ crosstalk as a novel mechanism enabling OSCC to exploit neural signals for PNI, highlighting a promising therapeutic target to block neural invasion and improve patient outcomes.

The novel anti-angiogenic inhibitor, KC1036, is effective in treating ES in the preclinical models.

Molecular docking confirmed a direct NOB-Npy1r interaction, while mechanistic analyses demonstrated modulation of the retinoic acid-related orphan receptors (RORs)/Bmal1-Yes-associated protein (Yap) pathway via Yap suppression and Bmal1 activation, based on the interventions with palmitic acid, BMS 193885 (Npy1r antagonist), and NPY. Therefore, this study provides evidence that NOB can protect β-cells from insulin secretion dysfunction by downregulating Npy1r expression and activating the RORs/Bmal1-Yap pathway.

Selective conditional activation of Wnt signalling and oncogenic Kras in combination with loss of TRP53 in these stem cell compartments resulted in the development of advanced, invasive cancers. This study establishes CreERT2 drivers as valuable tools for studying stem cell contributions to colon cancer.

Conversely, subtype C2 patients showed higher expression of NTRK2, STAT3, SIK1, AKT1, and EGFR, suggesting these genes as promising therapeutic targets for C2 subtype liver cancer. Furthermore, employing Weighted Correlation Network analysis, machine learning models, and experimental validation, we identified NPY1R and HGF as potential biomarkers for the diagnosis and treatment of liver cancer.

These findings suggest that CXCL9 and NPY1R could serve as predictive biomarkers for endocrine therapy response. Identifying these biomarkers may facilitate personalized treatment strategies, including the addition of therapies such as chemotherapy for resistant cases.

Pharmacological NPY1R inhibition in an intrasplenic model of PC metastasis recapitulated the results of our genetic studies, with BIBO3304 significantly decreasing liver metastasis. Together, our results reveal that NPY/NPY1R signaling is a previously unidentified antimetastatic target in PC.