ISG15 (ISG15 Ubiquitin Like Modifier)

High ISG15 expression within the G3/G4 MB subgroups correlates with prolonged survival, suggesting a potential tumor-suppressive function. These results collectively indicate that ISG15 may serve as a valuable prognostic biomarker for G3/G4 MB patients.

ISG15 in BRCA CSCs promotes lymph node metastasis by driving M2 macrophage polarization and suppressing T-cell activation, highlighting a critical role for ISG15-mediated immunomodulation and a potential therapeutic target.

Furthermore, we demonstrate that FASN knockout or FASN inhibitor treatment in myeloid cells abrogates the exaggerated tumor progression triggered by METTL3 knockout. Collectively, this study highlights the pivotal role of m6A in regulating macrophage metabolism and identifies potential targets in controlling GBM progression.

ISG15 is a newly identified target of AXL and may serve as a potential therapeutic target to overcome resistance in patients with NSCLC receiving AXL-targeted therapies.

Our investigation comprehensively characterized the cellular diversity and molecular features of the cervical cancer microenvironments.

KDM6A, a functional tumor suppressor, is frequently downregulated in OC. The KDM6A-ISG-15 axis is critical in restraining OC malignancy and may serve as a potential molecular target for novel therapies.

Mechanistically, our data suggest that ISG15 regulates Caspase-1 activity in DCs leading to lower IL-1 β secretion. In conclusion, this study reveals an essential role for ISG15 modulating DCs inflammatory activity and raises new questions regarding the specific mechanisms of how this protein regulates innate immune responses.

High ISG15 gene expression demonstrated significant correlations with QOL disturbances in fatigue, appetite loss and nutritional concern. These QOL factors could be capturing the anorexia-cachexia manifestations from interferon response induced by HCC.

These results nominate the S100A4-ISG15 axis as a central regulator of radiotherapy resistance and suggest that stratifying patients by S100A4-ISG15 expression or the "viral budding score" could predict radiotherapy resistance. Additionally, targeting this axis may offer an opportunity to overcome adaptive persistence in colorectal cancer and possibly other cancer types.

Together, our findings reveal that chronic ISG15 exposure promotes CD8+ T cell dysfunction, but these cells remain responsive to PD-1 blockade. This study identifies ISG15 as a potential biomarker for identifying patients likely to benefit from PD-1 blockade therapy.

Our findings demonstrate that hypoxic-induced M2 macrophages promote OS progression through OPN-dependent mechanisms, including inhibition of EGR3 and ISG15 expression and upregulation of RIG-I.

LUAD features a distinctive microbiota that engages with inflammatory and ceRNA regulatory pathways. These observations underscore the value of targeting microbiome-influenced mechanisms, such as the LCIIAR-ISG15 axis, as a promising approach to enhance treatment outcomes in lung adenocarcinoma.