AZM remits LPS-induced AKI by regulating M1 macrophage polarization via regulating ANXA1 and Notch1/NF-κB pathway. These findings may accelerate the translation of clinical drugs for the treatment of LPS-associated AKI.
Importantly, inhibition of CXCR2 effectively reverses ANXA1-mediated MDSCs infiltration. These results elucidate the essential function of ANXA1 in modulating the recruitment of MDSCs within the immune environment of NSCLC, establishing ANXA1 as a significant therapeutic target for the advancement of innovative immunotherapeutic approaches.
8 months ago
Journal • IO biomarker
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STING (stimulator of interferon response cGAMP interactor 1) • ANXA1 (Annexin A1) • CXCL5 (Chemokine (C-X-C motif) ligand 5) • CXCR2 (Chemokine (C-X-C motif) receptor 2) • UHRF1 (Ubiquitin Like With PHD And Ring Finger Domains 1)
These results suggest that the ANXA1/USP5/GOT1 axis promotes glutamine metabolism and ICC proliferation and growth. Inhibiting ANXA1 alongside glutamine uptake inhibition offers a promising strategy for treating ICC.
9 months ago
Journal
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ANXA1 (Annexin A1) • USP5 (Ubiquitin Specific Peptidase 5)
ANXA1 can promote the proliferation, migration and invasion of glioma; its expression is positively correlated with immune response and poor prognosis of glioma. The cancer-promoting mechanisms of ANXA1 in glioma and its correlation with the functional status of glioma patients warrant further investigation.
Plasma anti-ANXA1 and anti-MYC autoantibodies are likely to serve as a potential biomarker for clinical assessment of HCC prognosis, particularly in male patients.
Silencing Nrf2 abolished the Ac2-26-induced activation of NF-κB and cellular senescence in CHON-001 chondrocytes. Collectively, these findings offer new insights into the potential therapeutic use of Ac2-26 for treating OA.
On the basis of these results, it is reasonably speculated that targeting ANXA1 would provide an effective approach for treatment of AML. In support of this new therapeutic paradigm, provided proof-of-concept data by antagonizing ANXA1 using NICD inhibitory peptides.
The study demonstrated that a CAM subtype, CAM-A-induced formation of aberrant structures from HBV core protein aggregates in the nucleus leading to cell death by ANXA1-driven apoptosis. Thus, CAM-A treatment may lead to the specific elimination of HBV-infected cells by apoptosis, paving the way to novel therapeutic strategies for viral cure.
This research uncovers a novel role of macrophage ANXA1 in pancreatic cancer. ANXA1-mediated regulation of efferocytosis by tumor-associated macrophages promotes antitumor immune response via STING signaling, suggesting potential treatment strategies for pancreatic cancer.
These findings suggest that the infectious microenvironment induced by L. braziliensis affects the differentiation of M1 and M2 macrophages, cytokine release, and ANXA1 expression, thereby influencing the healing capacity of patients. Therefore, histopathological and immunological investigations may improve the selection of CL therapy.
We developed a simple and purification-free assay platform to isolate uEVs and quantitatively detect ECM1 and ANXA1 in uEVs by WGA-coupled magnetic beads and CLIA. Our results suggest that ECM1 and ANXA1 in uEVs could potentially serve as diagnostic biomarkers for breast cancer.