CXCL1 (Chemokine (C-X-C motif) ligand 1)

The antagonistic activity of that specific antagonist of TLR4 (TAK-242) (1 µmol·L-1), a specific TLR4 blocker, against S1 (10 µmol·L-1) was examined in co-cultured 16HBE cells and bone marrow-derived cells (BMDCs) or splenic lymphocytes (SLs) induced with LPS (1 µg·mL-1) to elucidate the TLR4 pathway's mediating role...S1's therapeutic effects occur through regulation of Th17/Treg immune cells and inflammation, attributable at least partially to the TLR4 pathway. This study provides molecular justification for S1 in AA treatment.

Gemcitabine/Cisplatin (Gem/Cis) chemotherapy is a standard treatment for muscle-invasive bladder cancer (MIBC) but yields suboptimal response rates. Using TCGA bladder cancer data, the transcriptomic gene set was further validated revealing a prognostic signature associated with patients' outcome. These findings uncover a novel mechanism of chemotherapy resistance in bladder cancer driven by tumor-stromal interactions and macrophage recruitment and suggest that targeting macrophage infiltration may improve chemotherapy response in bladder cancer.

Serum was collected from hypertensive patients treated with amlodipine, nebivolol, and perindopril for 6 weeks, alongside samples from healthy individuals. In summary, our study demonstrates that antihypertensive therapy, especially with nebivolol, potentially reverses hypertension-induced changes that exacerbate the cancer-promoting phenotype of endothelial cells. This suggests that beyond controlling blood pressure, antihypertensive treatments may also play a role in modulating cancer progression.

These polarized macrophages further enhance tumor cell proliferation and invasion, thereby forming a tumor-immune feedback loop. In conclusion, this study clarifies how IL7R signaling mediates crosstalk between ovarian cancer cells and macrophages to maintain the homeostasis of the immunosuppressive tumor microenvironment (TME).

Biophysical assays, including surface plasmon resonance (SPR), Schild analysis, and competitive ELISA, confirmed direct competition of IRA10L with IL-36 ligands for receptor binding. These findings establish IRA10L as a specific, competitive IL-36R antagonist, highlighting its potential as a targeted therapeutic for IL-36-mediated inflammation and cancer and providing a foundation for future drug development.

Bile acids and the microbiota are necessary for duodenal adenoma development and are potentially modifiable risk factors in humans at risk of duodenal adenomas. The recruitment of myeloid cells may promote tumor progression via the release of reactive oxygen species.

Clinically, G-/granulocyte-macrophage colony-stimulating factor (GM-CSF) adjuvants and G-CSF-mobilized granulocyte transfusion offer context-dependent benefits yet pose toxicity risks, underscoring the need for precise intervention in neutrophil activation. Advances in single-cell and spatial multi-omics approaches are uncovering the metabolic and functional heterogeneity of neutrophils within mucosal environments, providing mechanistic insight for targeted immunomodulation.

Clinical sample analysis revealed that FASN protein expression was significantly positively correlated with the levels of HK2, lactate, and H3K18la, thereby validating the clinical relevance of this regulatory pathway. In conclusion, HB-derived exosomal FASN affected the transformation of LX2 cells into CAFs by regulating the stability of HK2 and mediating histone lactylation, providing novel insights into the crosstalk between HB cells and CAFs and highlighting exosomal FASN as a potential therapeutic target for HB.

To overcome these barriers, a pH-responsive solid lipid nanoparticle (SLN) system was engineered to co-deliver CB-5083 (a VCP/p97 inhibitor), miR-142 (a PD-L1-targeting microRNA), and imiquimod (R, a TLR7 agonist) for spatially confined induction of endoplasmic reticulum stress (ERS) and immune reprogramming in MSS CRC. Biodistribution analysis confirmed tumor-preferential accumulation with minimal off-target exposure, and biosafety profiling demonstrated low systemic toxicity. This TME-responsive nanoplatform therefore integrates ERS induction, checkpoint modulation, and cytokine suppression to overcome immune exclusion in MSS CRC, representing a clinically translatable strategy for chemo-immunotherapy in immune-refractory tumors.

The cyst-derived stromal cells exhibited early chromosomal instability and overexpression of MMP1 and PAPPA, supporting their potential role in ovarian carcinogenesis. These immortalized stromal cell lines provide a novel and stable platform for mechanistic studies and may contribute to biomarker discovery and therapeutic target development in ovarian cancer.

Our comprehensive profiling of ORF74 chemokine ligands reveals ligand-dependent activation of canonical signaling pathways, including calcium mobilization, β-arrestin recruitment and chemotaxis. We confirm that ORF74 exhibits constitutive β-arrestin recruitment and, upon co-expression with CXCR4, is able to modulate CXCL12-CXCR4-mediated cell migration. These data highlight the complex chemokine-ORF74 interplay and will contribute to a better understanding of KSHV infection and pathology through multiple ORF74-dependent mechanisms.

Furthermore, either siCXCL1 or FTO inhibition markedly inhibited CUMS-induced BC progression, accompanied by suppression of adipocyte lipolysis, ROS production, and mitochondrial fission, as well as KEAP1 m6A demethylation. Our findings highlight the novel signaling of TRP/TAM/CXCL1 in mediating adipocyte lipolysis underlying CUMS-induced BC progression, and KEAP1 m6A demethylation presents a promising therapeutic target.