IL3 (Interleukin 3)

Actinomycin D treatment combined with RT-qPCR was used to assess ILF3 mRNA stability...In vivo, DDX3X inhibitor, RK-33, markedly inhibited NB tumor growth and metastasis and enhanced M1 macrophage polarization, which was partially reversed by ILF3 overexpression. DDX3X promotes NB progression by stabilizing ILF3 mRNA, thereby facilitating M2 macrophage polarization.

These data suggest high IL33/ST2 levels are significant poor prognostic factors for nivolumab therapy for advanced GC. The IL33/ST2 axis may be useful as a biomarker for predicting and pre-selecting possible responders/nonresponders to anti-PD1/PDL1 therapy for GC, and hopefully as a druggable target for developing new drugs for treating GC. The IL33/ST2-targeting strategy will contribute to improving clinical outcomes in the treatment of GC.

This resulted in increased ILF3 levels that counteracted ferroptosis. In summary, our study underscores the oncogenic function of ILF3 in CRC and suggests that ILF3 knockdown may serve as a promising therapeutic approach for CRC.

In conclusion, our research has revealed a novel role for ILF3 in controlling lipid metabolism, specifically through its interaction with CPT1A mRNA in the PPARα signaling pathway. This discovery offers a conceptual basis for further exploring the pathological mechanism of PC.

Tumor-derived ILT3 overexpression suppresses anti-tumor immunity by recruiting M2-like TAMs and impairing T cell activities, while ILT3 inhibition counteracts this immunosuppression and enhances the efficacy of PD-L1 blockade in LUAD. Thus, ILT3 could be a promising novel immunotherapeutic target for combined immunotherapy.

Next-generation sequencing and Kyoto Encyclopedia of Genes and Genomes analysis revealed that ILF3 regulated PD-L1 expression through the DEPTOR/mTOR signaling pathway. Overall, simvastatin induced ferroptosis in GC cells by inhibiting ILF3 expression while promoting the activation of CD8+ T cells to augment antitumor immune responses, thereby facilitating synergistic immunotherapy.

NOG (NOD/Shi-scid/IL-2Rγnull) and NOG-EXL (huGM-CSF/huIL-3 NOG) mice conditioned with busulfan underwent i.v. injection of human CD34+ cells...In this context, animal models that recapitulate human disease are greatly needed. Leveraging xenograft tumors derived from patients with unresectable HCCs and a commercially available immunodeficient mouse strain that expresses human GM-CSF and IL-3, we demonstrate a novel but accessible approach for modeling the HCC tumor microenvironment.

ILF3 promotes the evolution of NAFLD by inhibiting the expression of p-AMPK. The knockdown of ILF3 activates the AMPK signaling pathway, alleviating the severity of NAFLD. These findings underscore the function of ILF3 in the pathogenesis of NAFLD and demonstrate its viability as a treatment focus and diagnostic indicator.

Melatonin mitigates IA injury by modulating immune cells and hypoxia-related factors. These findings provide an exploratory foundation for therapeutic strategies in IA.

Importantly, selective knockout of Prtn3 in macrophages significantly enhanced the antitumor effect of anti-PD1 therapy in the mouse model of LUAD. Thus, our work demonstrated that PRTN3 in macrophages, served as a key immunoregulator, contributed to impede the antitumor immune response through reinforcing the TAMs/Tregs crosstalk, which provided valuable insights to improve the immunotherapeutic effect by functional remodeling of TAMs to alleviate immunosuppression in LUAD.

In our case of CEL with the ETV6::RAPGEF6 fusion, we also demonstrated overexpression of IL3, which could potentially result from the proximity of the IL3 gene to RAPGEF6, similar to what is observed with ACSL6 and IL3. The use of RNA sequencing in routine diagnosis of CEL could provide evidence for clonal event such as gene fusion, improving diagnosis as well as prognosis and therapeutic approaches.

Our results showed that the inhibition of Brd4 suppressed IFNγ-induced cytotoxicity by modulating the Jak-Stat pathway. These data suggested that the inhibition of Brd4 could increase cell viability in the cancer microenvironment where IFNγ is abundant, revealing a new aspect of the molecular mechanism of CRC development. Our results may help in evaluating the application of Bet inhibitors in treating CRC. Additionally, our RNA-seq data sets will be helpful for clarifying the relationship between Brd4 and immunomodulators, such as Il33, or for studying the responses of colonic epithelial cells to IFNγ.