S100A8 expression

The signature of CAL effects is detected in the bone marrow progenitors of patients with myeloid malignancy or severe infection. These results position CAL as a mediator of IL6 effects on triggering anemia during inflammation, an effect that is amplified in the context of JAK2-V617F-driven hematopoiesis.

S100A8 promotes tumor progression by inducing phenotypic polarization of microglia through the TLR4/IL-10 signaling pathway in glioma. It might represent a therapeutic target for further basic research or clinical management of glioma.

The findings suggested that patients with high KDELR2 expression might benefit from immune checkpoint therapy. KDELR2 was also shown to enhance bladder cancer cell proliferation, invasion, and migration, highlighting it as a promising target for macrophage-focused drug development.

Our findings reveal that CCN1 may be an important factor in the enhanced invasiveness and MES phenotype transition of GSCs and highlight the potential to target CCN1 for treating GBM.

In summary, this study substantiates the therapeutic potential of QSXZ and its primary active compound CTS, as promising alternative treatments for GA. Our findings provide valuable insight into the critical pharmacological mechanism of QSXZ in regulating inflammation, highlighting its potential therapeutic effects in GA management.

Our study represents the first investigation into the role of IL-37d in inhibiting tumor metastasis during the early stages by suppressing S100A8/9 and MMP9 expression in lung tissue, thereby reducing neutrophil recruitment and spontaneous migration from the bone marrow.

The estrogen receptor status was positive in patients with high levels of the S10014 gene, but negative in S100A2, S100A8, and S100A9 expression levels. Cell dependence needs to be considered while designing new breast cancer treatments since gene signatures might vary depending on the type of tumor.

By focusing on S100A8 as a therapeutic target, we identified at least three multivalent S100A8 inhibitory peptides. Here, we review the tumor-promoting role of S100A8-mediated TLR4 signaling and propose S100A8 as a potential therapeutic target for aggressive cancer.

S100A8/A9 may be a promising marker for the diagnostic and prognostic assessment of the HNSCC patients. Based on these insights, we have devised a new classification model for HNSCC, which has the potential to enhance the management and personalized treatment of HNSCC patients. The model should also be further optimized through the expansion of sample size and implemented experimental studies in future research.

Fluorescent immunohistochemistry revealed that S100A9 and S100A8 were expressed in alveolar epithelial cells and neutrophils in indium-exposed rats. These results suggest that S100 proteins contribute to indium-induced lung diseases via neutrophil-mediated inflammatory responses.

High expression of RNF7 in NSCLC cells promotes CXCL1 expression by activating the NF-κB signaling pathway, thus leading to the chemotactic recruitment of MDSCs, which contributes to tumor resistance to antiPD-1 therapy.

In this work, we reviewed our current understanding of S100A8/A9 overexpression in inflammation and its importance in the development and progression of CNS inflammatory diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), and stroke, and the functional roles and therapeutic applications of S100A8/A9 in these diseases. Finally, we discussed the current barriers and future research directions of S100A8/A9 in CNS diseases.