IL1A (Interleukin 1, alpha)

Trogocytosis-related CLDN18.2 inhibited the glucose uptake, glycolysis and cytotoxicity of tumour-infiltrating CD8+ T cells by promoting the ubiquitin-proteasomal degradation of β-catenin in PDAC. Therefore, targeting trogocytosis-related CLDN18.2+CD8+ T cells may be a promising therapeutic strategy to inhibit PDAC progression.

We developed a viable in vitro model to study contact-compression, showing biomechanical inflammatory and remodeling responses. With adjustable components, this model can be applied to further study tissue responses to lung implants.

Key prognostic genes, including SLC2A1, SLC16A1, IL1A, AHSG, and ALOX15, were validated through RT-qPCR. This study highlights the molecular heterogeneity of propionate metabolism in LUAD and proposes a prognostic signature that could inform immunotherapeutic stratification.

Low levels of miR-323b-5p predict a poor prognosis for NSCLC. miR-323b-5p regulates the cell cycle of NSCLC cells by targeting IL1A, thereby inhibiting cell proliferation.

Targeting the phenotypic transformation of glial cells, repairing the BBB, or modulating glial cell metabolism (e.g., lactate shuttle) may represent potential strategies requiring further validation. Future research should focus on the spatiotemporal dynamics of this axis and its clinical translation.

Our findings identify PRDM1 as a key factor associated with nICRT resistance and suggest that targeting ferroptosis pathways or disrupting PRDM1+ cell-mediated immune suppression may represent a viable strategy in ESCC. Clinical trial registration number: NCT03940001.

Macrophages from Il1α⁻/⁻ tumors exhibited activated immune gene signatures similar to human macrophages. These findings reveal that IL-1α drives an immunosuppressive TME partly through PGE2 signaling, highlighting IL-1α as a potential therapeutic target in breast cancer.

Utilizing a panoptosis gene set, this study identified eight core genes involved in hepatic IRI, providing novel insights into panoptosis' role in hepatic IRI.

These findings highlight IL-1α, IL-12 and TGF-β1 as promising tissue biomarkers of aggressive PeCa and support a central role for cytokine-driven immune dysregulation in penile cancer. The prognostic value of IL-12 should be considered exploratory and warrants validation in larger, multicentre cohorts.

However, depletion and supplementation assays clearly show that the presence of these specific cytokines is critical to induce a migratory phenotype and that naïve Cal27's motility is regulated by MAPK and AKT signaling pathways; loss or inhibition of these pathways reduced migration. These data suggest that paracrine signals from stiffness-induced mesenchymal cells act via distinct kinase pathways and may be necessary for cooperative dissemination of OSCC.

Additionally, ELISA validation showed that the key protein CINC-2 was upregulated and CNTF was significantly downregulated in the early CCI group. The progression of early sciatic is closely associated with neuroinflammation triggered by the overexpression of inflammatory factors and nerve dysfunction mediated by neurotrophic-related proteins.

Furthermore, single cell and spatial transcriptomics reinforces the role of APOBEC3A in fostering squamous trans-differentiation and promoting the emergence of a subpopulation of highly squamous epithelial cells. Our results demonstrate that mouse Apobec3 and human APOBEC3A promote squamous differentiation in urothelial carcinoma and that this trans-differentiation phenotype is mediated through IL-1α signaling, a target of FDA approved therapies for rheumatologic disease.