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Pro- and anti-tumorigenic capacity of immunoproteasomes in shaping the tumor microenvironment

ABSTRACT: Pro- and anti-tumorigenic capacity of immunoproteasomes in shaping the tumor microenvironment

PROVIDER: PRJNA634311 | ENA |

REPOSITORIES: ENA

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Pro- and anti-tumorigenic capacity of immunoproteasomes in shaping the tumor microenvironment

Project description:Apart from the constitutive proteasome, the immunoproteasome that comprises the three proteolytic subunits LMP2, MECL-1 and LMP7 is expressed in most immune cells. In this study we describe two opposing roles for immunoproteasomes in regulating the tumor microenvironment. During chronic inflammation, immunoproteasomes modulated the expression of pro-tumorigenic cytokines and chemokines and enhanced infiltration of innate immune cells that led to the onset of colitis-associated carcinogenesies (CAC). In ulcerative colitis (UC) patients with high risk for CAC, immunoproteasome-induced pro-tumorigenic mediators were highly upregulated. Interestingly, the role for the same enzymatic complex in melanoma tumors is relatively unknown. We found that the high expression of immunoproteasomes in human melanoma was associated with better prognosis. Our data revealed that the immunoproteasome has a strong anti-tumorigenic function in cancer types with non-inflammatory microenvironment such as melanoma. CD8+ cytotoxic T lymphocytes (CTLs) from immunoproteasome-deficient mice were reduced during T cell homeostasis and were not able to combat melanoma efficiently. Our results indicate that the immunoproteasome exhibits either pro- or anti-tumoral properties in a context-dependent manner.

2021-08-18 | GSE150979 | GEO

Tumor-initiating stem cell shapes its microenvironment into an immunosuppressive barrier and pro-tumorigenic niche

Project description:Tumor-initiating stem cell shapes its microenvironment into an immunosuppressive barrier and pro-tumorigenic niche

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Mutant p53 elicits context-dependent pro-tumorigenic phenotypes

Project description:Mutant p53 elicits context-dependent pro-tumorigenic phenotypes

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Pro- and Antitumorigenic Capacity of Immunoproteasomes in Shaping the Tumor Microenvironment.

Project description: Not available

| S-EPMC8355016 | biostudies-literature

Tumor-initiating stem cell shapes its microenvironment into an immunosuppressive barrier and pro-tumorigenic niche

Project description:Tumor-initiating stem cells (TSCs) are critical for drug resistance and immune escape. However, the mutual regulations between TSC and tumor microenvironment (TME) remain unclear. Using DNA-label retaining, single-cell RNA sequencing (scRNA-seq), and other approaches, we investigated intestinal adenoma in response to chemoradiotherapy (CRT), thus identifying therapy-resistant TSCs (TrTSCs). We find bidirectional crosstalk between TSCs and TME using CellPhoneDB analysis. An intriguing finding is that TSCs shape TME into a landscape that favors TSCs for immunosuppression and propagation. Using adenoma-organoid co-cultures, niche-cell depletion, and lineaging tracing, we characterize a functional role of cyclooxygenase-2 (Cox-2)-dependent signaling, predominantly occurring between tumor-associated monocytes and macrophages (TAMMs) and TrTSCs. We show that TAMMs promote TrTSC proliferation through prostaglandin E2 (PGE2)-PTGER4(EP4) signaling, which enhances β-catenin activity via AKT phosphorylation. Thus, our study shows that the bidirectional crosstalk between TrTSC and TME results in a pro-tumorigenic and immunosuppressive contexture.

2021-07-02 | GSE136256 | GEO

Mutant p53 elicits context-dependent pro-tumorigenic phenotypes (microarray)

Project description:Mutant p53 elicits context-dependent pro-tumorigenic phenotypes (microarray)

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Mutant p53 elicits context-dependent pro-tumorigenic phenotypes (ChIP-Seq)

Project description:Mutant p53 elicits context-dependent pro-tumorigenic phenotypes (ChIP-Seq)

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Proteolytic processing converts pro-tumorigenic Angiopoietin-like 4 into an inhibitor of metastasis

Project description:Preclinical and clinical studies have solidly established the concepts of concomitant tumor resistance (CTR), the inhibition of metastases formation by the primary tumor. Yet, the mechanisms of CTR are poorly understood and bench-to-bedside studies are largely missing. Here, we show that proteolytic processing of ANGPTL4 liberated the potent CTR-inducing capacity of the N-terminal cleavage fragment, nANGPTL4. Full-length ANGPTL4 was primarily detected in tumor tissues, whereas nANGPTL4 predominated in the systemic circulation, whose concentrations correlated inversely with disease progression. Comparative studies in multiple preclinical tumor models revealed distinctly opposing functions of the ANGPTL4 cleavage fragments. Full length and cANGPTL4 promoted tumor growth and metastasis leading to reduced overall survival. Conversely, nANGPTL4 inhibited metastasis formation and enhanced overall survival. The experiments identified proteolytic cleavage as regulatory mechanism converting pro-tumorigenic ANGPTL4 into anti-metastatic nANGPTL4. Moreover, the results revitalize the concept that primary tumors may suppress metastases through systemic release of metastasis-inhibiting cytokines

2022-10-17 | PXD020269 | Pride

Transcription profiling of hepatic tissues from mice exposed to PB, propiconazole (Pro) or triadimefon (Tri) at tumorigenic exposure levels

Project description:The goal of this study was to apply transcriptional analyses to hepatic tissues from mice exposed to PB, propiconazole (Pro) or triadimefon (Tri) at tumorigenic exposure levels to reveal similarities and differences in response among these treatments.The goal of this study was to apply transcriptional analyses to hepatic tissues from mice exposed to PB, propiconazole (Pro) or triadimefon (Tri) at tumorigenic exposure levels to reveal similarities and differences in response among these treatments. Experiment Overall Design: Briefly, male CD-1 mice received propiconazole (2500 ppm), tridimefon (1800 ppm), or phenobarbital (850 ppm) in the feed or, control feed for periods of 4 and 30 days. This resulted in an average daily intake of 349.6 Â± 46.7 of propiconazole, 257.1 Â± 33.5 of tridimefon or 97.2 Â± 5.9 mg/kg/day of phenobarbital.

2009-07-05 | E-GEOD-16777 | biostudies-arrayexpress

Proteolytic inactivation of the autoinhibitory prodomain is essential for the pro-tumorigenic function of membrane type-1 matrix metalloproteinase (MT1-MMP)

Project description:Invasive cancers employ pericellular proteolysis to breach the extracellular matrix and basement membrane barriers and invade the surrounding tissue. Pro-invasive, pro-tumorigenic MT1-MMP is the primary mediator of proteolytic events on the cancer cell surface. Cellular MT1-MMP is synthesized as a latent zymogen. The latency of MT1-MMP is maintained by its N-terminal inhibitory prodomain. Our study reveals a critical mechanism underlying the activation pathway and subsequent execution of the tumor-promoting function of MT1-MMP. Evidence suggests that the prodomain undergoes intradomain cleavage at the PGD↓L50 cleavage site followed by the release of the degraded prodomain by furin cleavage of the R108RKR111↓Y112 site. These events, only if combined, cause the activation of MT1-MMP. The significance of these molecular events to the pro-tumorigenic function of MT1-MMP in malignancy remained, however, unidentified. To identify the functional importance of the PGD↓L50 intradomain cleavage in the activation and tumorigenic program of MT1-MMP, our current studies employed the cells which expressed the wild-type prodomain-based fluorescent biosensor and the mutant biosensor with the inactivated PGD↓L50 cleavage site (L50D mutant) and also the cells with the enforced expression the wild-type and mutant MT1-MMP. Using cell-based tests and orthotopic breast cancer xenografts in mice, we demonstrated that the intradomain cleavage of the PGD↓L50 sequence of the prodomain is essential for the pro-tumorigenic function of MT1-MMP. Our study contributes to the growing consensus for the design of selective, precisely focused MT1-MMP inhibitors in cancer. Analysis of global gene expression in orthotopic tumor and cultured breast cancer cells expressing wild-type and mutant Mt1-MMP forms

2011-06-01 | E-GEOD-28655 | biostudies-arrayexpress

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