STAT1 (Signal Transducer And Activator Of Transcription 1)

Collectively, these findings indicate that CEP55 promotes liver cancer immune escape and malignant progression through modulation of STAT1-dependent PD-L1/MHC-I expression, oxidative stress, and immunosuppressive signaling. Targeting CEP55 may therefore represent a potential strategy to improve antitumor immune recognition in liver cancer.

Our findings highlight a strong association between the upregulation of PDAC recurrence genes and the activation of metabolic pathways linked to obesity, diabetes, and inflammation. The consistent expression patterns across species suggest potential for developing targeted therapies to inhibit these metabolic pathways post-pancreatic cancer resection, potentially reducing fatality.

Mechanistically, LGMN binds to integrin αvβ3 on the macrophage surface and restrains M1 polarization by inhibiting the mechanistic target of rapamycin complex 1 (mTORC1)/signal transducer and activator of transcription 1 (STAT1) pathway...These findings reveal the pivotal role of LGMN in restraining sarcoid granulomatous inflammation through suppression of mTORC1/STAT1-driven M1 macrophage polarization. Therefore, LGMN supplementation may be a promising therapeutic strategy for sarcoidosis.

This study characterizes CX3CR1+CD8+T cells as a key effector subset predicting prognosis and immunotherapy response in colorectal cancer. These insights not only support their use as a clinically meaningful biomarker but also highlight the regulatory network orchestrated by ETS1 and PRDM1 as a promising avenue for overcoming immune resistance.

These findings identify Niclosamide as a potent dual STAT1/STAT3 inhibitor capable of reversing IFN-γ- and hypoxia-driven immune evasion. Repurposing Niclosamide may represent a promising strategy to enhance the efficacy of immune checkpoint blockade in solid tumors.

LDs play key roles in disease initiation or progression, including autoimmunity or cancer, as well as chronic inflammatory diseases due to their role in (1) lipotoxicity, (2) cell death regulation, (3) immune system amelioration, and (4) energy provision. Finally, the therapeutic consequences of the angles are outlined, along with future research directions.

Furthermore, dual luciferase reporter analysis demonstrated that STAT1 directly binds to and activates the IFN-γR1 promoter, establishing a potential feedback loop. Our findings demonstrate that ST6Gal1 governs ESCC resistance to IFN-γ by modulating the STAT1-dependent transcription of IFN-γR1.

Myeloid cells exhibited expression of immunomodulatory genes (RUNX3, DDIT4, IL4I1), and malignant T-cells expressed exhaustion-associated markers (CXCL13, SOCS3, F2R, ETV1), as opposed to AD and healthy control samples. Thus, our results provide a novel insight into the immune-stroma crosstalk in the tissue microenvironment of early-stage MF vs. AD skin lesions.

Mechanistically, RUNX1 interacts with STAT1 to inhibit its dimerization and subsequent transcriptional activation of GITRL, thereby suppressing GITRL expression. Our findings highlight the RUNX1/STAT1/GITRL axis as a potential therapeutic target for GITR-based immunotherapy in CRC.

MCP-1 was secreted from macrophages interacted with the CCR2 receptor on prostate cancer cells, thereby activating the JAK/STAT1 pathway, ultimately contributing to the progression of prostate cancer and its resistance to radiotherapy. Taken together, our findings identified a STAT1/lactate/NFκB1/MCP-1 positive feedback mechanism as a driver of prostate cancer progression and resistance to radiotherapy that functioned by interaction to macrophages, which could be potential therapeutic targets for the advanced prostate cancer.

In patient-derived xenograft models, co-treatment with FLT3i (quizartinib) and CD276-targeting agents led to 72.9%-80.4% tumor burden reduction and enhanced CD8+ T cell function, outperforming quizartinib monotherapy. These findings define a scaffolded PKCι-pS727-STAT1 signaling axis that promotes immune evasion in FLT3-ITD AML, supporting combined FLT3 and CD276 targeting as a promising translational strategy in this aggressive leukemia subtype.