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Targeting PGLYRP1 promotes anti-tumor immunity while inhibiting autoimmunity

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE223896 | GEO | 2023/06/09

REPOSITORIES: GEO

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Targeting cathepsin B by cycloastragenol enhances anti-tumor immunity via inhibiting MHC-1 degradation and promoting the presentation of tumor antigen

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Targeting IRE1α reprograms the tumor microenvironment and enhances anti-tumor immunity in prostate cancer

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FLI1 promotes IFN-γ-induced kynurenine production to impair anti-tumor immunity

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ARIH1 signaling promotes anti-tumor immunity by targeting PD-L1 for proteasomal degradation.

Project description:Cancer expression of PD-L1 suppresses anti-tumor immunity. PD-L1 has emerged as a remarkable therapeutic target. However, the regulation of PD-L1 degradation is not understood. Here, we identify several compounds as inducers of PD-L1 degradation using a high-throughput drug screen. We find EGFR inhibitors promote PD-L1 ubiquitination and proteasomal degradation following GSK3α-mediated phosphorylation of Ser279/Ser283. We identify ARIH1 as the E3 ubiquitin ligase responsible for targeting PD-L1 to degradation. Overexpression of ARIH1 suppresses tumor growth and promotes cytotoxic T cell activation in wild-type, but not in immunocompromised mice, highlighting the role of ARIH1 in anti-tumor immunity. Moreover, combining EGFR inhibitor ES-072 with anti-CTLA4 immunotherapy results in an additive effect on both tumor growth and cytotoxic T cell activation. Our results delineate a mechanism of PD-L1 degradation and cancer escape from immunity via EGFR-GSK3α-ARIH1 signaling and suggest GSK3α and ARIH1 might be potential drug targets to boost anti-tumor immunity and enhance immunotherapies.

| S-EPMC8058344 | biostudies-literature

Transcription factor Ikzf1 associates with Foxp3 to repress gene expression in Treg cells and limit autoimmunity and anti-tumor immunity

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BET Inhibition Enhances TNF Mediated Anti-Tumor Immunity

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Fibrinogen promotes autoimmunity and demyelination via chemokine release and antigen presentation

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CDK4/6 inhibition promotes anti-tumor immunity

Project description:Pharmacologicalinhibitors of cyclin dependent kinases 4 and 6 (CDK4/6) are an approvedtreatment forhormone receptor-positive breast cancer and are currently under evaluation across hundreds of clinical trials for other cancertypes. The clinical success of these inhibitorsis largely attributedto well-defined tumor-intrinsic cytostatic mechanisms, while their emerging role as immunomodulatory agents is lessunderstood. Usingintegrated epigenomic, transcriptomic and proteomicanalyses, we demonstrateda novel action of CDK4/6inhibitorsin promoting the phenotypic and functional acquisition of immunological T cell memory.Short-term priming with a CDK4/6inhibitorpromoted long-termendogenousanti-tumor T cell immunityin mice, enhanced the persistence and therapeutic efficacy of chimeric antigen receptor (CAR)-T cells, and induced an RB-dependent T cell phenotype supportive offavorable responses to immune checkpoint blockade in melanoma patients.Together, thesemechanistic insights significantlybroaden the prospective utility of CDK4/6 inhibitors as clinical tools to boostanti-tumorT cell immunity.

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Plinabulin, a Distinct Microtubule-Targeting Chemotherapy, Promotes M1-Like Macrophage Polarization and Anti-tumor Immunity

Project description:Reprogramming tumor infiltrating myeloid cells to elicit pro-inflammatory responses is an exciting therapeutic maneouver to improve anti-tumor responses. We recently demonstrated that a distinct microtubule-targeting drug, plinabulin—a clinical-stage novel agent—modulates dendritic cell maturation and enhances anti-tumor immunity. Here, we investigated the effects of plinabulin on macrophage polarization in vitro and in vivo. Plinabulin monotherapy induced significant tumor growth inhibition in mice bearing subcutaneous MC38 colon cancer. Importantly, the regressing tumors were characterized by an increase in M1-like/M2-like tumor-associated macrophages (TAM) ratio. The efficacy of plinabulin remained unaltered in T cell-deficient Rag2?/? mice, suggesting an important role of macrophages in driving the drug's anti-tumor effect. Exposure of murine and healthy human macrophages to plinabulin induced polarization toward the M1 phenotype, including increased expression of co-stimulatory molecules CD80, CD86 and pro-inflammatory cytokines IL-1?, IL-6, and IL-12. M2-associated immunosuppressive cytokines IL-10 and IL-4 were reduced. This pro-inflammatory M1-like skewing of TAMs in response to plinabulin was dependent on the JNK pathway. Functionally, plinabulin-polarized human M1 macrophages directly killed HuT 78 tumor cells in vitro. Importantly, plinabulin induced a functional M1-like polarization of tumor infiltrating macrophages in murine tumors as well as in tumor samples from ovarian cancer patients, by preferentially triggering M1 proliferation. Our study uncovers a novel immunomodulatory effect of plinabulin in directly triggering M1 polarization and proliferation as well as promoting TAM anti-tumoral effector functions.

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