TNFSF10 (TNF Superfamily Member 10)

In addition, TNFSF10-mediated PANoptosis may facilitate preeclampsia progression by promoting inflammation through NK cell activation and M1 macrophage polarization at the maternal-fetal interface. Our findings not only establish TNFSF10 as a critical mediator of placental PANoptosis, but also reveal its dual role in coordinating trophoblast cell death and immune dysregulation, suggesting novel therapeutic strategies targeting preeclampsia.

Effect size estimates were relatively large for both the group effect (partial η2=0.20) and the time x group interaction (partial η2=0.24), suggesting that the study may have been underpowered to detect this difference statistically. In conclusion, the present exploratory study suggests that suramin exerts a dual antitumor effect on tongue squamous cell carcinoma by suppressing proliferative transcriptional programs, and modulating extracellular and stress response pathways, providing a basis for future studies to further elucidate its therapeutic relevance.

The expressions of STAT3, N-cadherin, and CDK2 proteins were down-regulated, and the expressions of GPX3 and TNFSF10B were up-regulated. This study provides a comprehensive understanding of the molecular mechanisms underlying U(VI)-induced pulmonary epithelial cytotoxicity.

Most significantly, FB.TNFSF10 abundance emerged as a robust predictor of immune checkpoint inhibitor therapy resistance across multiple cancer cohorts, independent of conventional biomarkers. This biofabrication platform provides a scalable, reproducible framework with broad applicability beyond oncology. The systematic optimization methodology is readily adaptable to other tissue types, disease models, and high-throughput drug screening applications, representing a significant advancement in functional tissue engineering for precision medicine.

Receiver Operating Characteristic (ROC) and Hazard Ratio (HR) analyses demonstrated that the biomarker score was correlated with response to anti-PD-1 therapy in a cohort of kidney cancer patients and correlated with better overall survival (OS) in cancer patients treated with anti-programmed death-ligand 1 (PD-L1) and anti-cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) therapies. In summary, we have identified a transcriptional biomarker that predicts cellular response to PARP7i and AHRa combination therapy which is associated with benefits from immune checkpoint inhibitor (ICI) therapies in cancer patients.

This study presents an innovative immune dictionary approach to identify key immune- and mitochondria-related DEGs in PAAD, providing potential targets for new therapeutic strategies and personalized treatment approaches. .

Notably, MDK treatment drives tumor cells into the cell cycle, thereby increasing the therapeutic effect of busulfan. Furthermore, MDK promotes osteogenic differentiation of mesenchymal stem cells (MSC), contributing to the remodeling of the bone marrow microenvironment. In addition, type I IFN upregulates TNFSF10, leading to tumor cell death through mutual killing.

Although direct cytotoxic effects were not observed in co-culture experiments, the absence of increased leukemic cell growth under any priming condition supports the biological safety of this approach. These findings provide a strong foundation for further in vivo studies to assess the therapeutic applicability of primed MSCs in hematologic malignancies while ensuring oncologic safety.

Collectively, TGFβ1+ Treg may mediate CD8+ T cell dysfunction through these ligand-receptor interactions, accelerating T cell exhaustion and apoptosis, thereby fostering a profoundly immunosuppressive tumor microenvironment that ultimately drives CRC immune evasion and malignant progression.

These findings demonstrate a critical role for TNF superfamily signaling in stem cell maintenance. Zebrafish tnfrsfa maintains the stem cell niche in neuromasts and is necessary for hair cell regeneration of the lateral line Tnfrsfa is essential for mantle cell proliferation during lateral line development and hair cell regenerationTnfsf10 and Tnfsf10l3 signal through Tnfrsfa, activating NF-κB signaling and Sox2 expression in the mantle cells in a non-cell-autonomous mannerTnfrsfa regulates the development of neuromast independently of the Notch signaling pathway.

The risk score greatly differed with the different expression levels of key immune checkpoints and immune cell infiltration, and the levels of immune cells were higher in the low-risk group. In this study, bioinformatic analysis proved that immune-a1-related genes could be used to distinguish between normal and COADREAD specimens and that immunity and autophagy are associated with low-risk COADREAD; therefore, these genes have the potential to improve clinical predictions of COADREAD risk.

TRAIL was identified as a direct transcriptional target of HIF2α and paradoxically found to be crucial for cell proliferation, primarily by activating the p38 MAPK pathway and facilitating G1/S phase transition. Depletion of endogenous TRAIL or inhibition of HIF2α with belzutifan sensitizes ccRCC cells to recombinant TRAIL, presenting a promising avenue for combination therapy to overcome both TRAIL resistance and belzutifan resistance in treating ccRCC.