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Education of tumour-associated macrophages by the tumour matrisome inhibits immune surveillance

ABSTRACT: Education of tumour-associated macrophages by the tumour matrisome inhibits immune surveillance

PROVIDER: PRJNA772736 | ENA |

REPOSITORIES: ENA

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Education of tumour-associated macrophages by the tumour matrisome inhibits immune surveillance

Project description:Metastatic ovarian tissues represent a complex tumour microenviroment. We analysed the tumour matrisome and immune cell environment in 39 metastatic ovarian tissues. We developed a disease score system, which positively correlated with the tumour matrisome. A distinct matrisome signature was identfied with increasing disease. Immune abundance and phenotype positively correaletd with tumour matrisome components. We developed a decellularised tissue model using metastatic ovarian omental tissues that maintained ECM protein content and architecture and cultured human blood-derived macrophages derived from four different donors. Monocytes cultured on high diseased tissues differerntiated into a distinct macrophage population, different from uninvovled (low disease) samples. Tumour ECM cultured macrophages had pro-tumorgenic phenotype and function.

2023-03-24 | GSE186145 | GEO

Temporal Profiling of PyMT Tumour Matrisome during Progression

Project description:In this study, through coupling of our ISDoT tissue decellularisation technology with quantitative mass spectrometry, we explored the changing tumour matrisome during mammary tumourigenesis in the PyMT breast cancer model compared to age-matched healthy control mammary gland

2022-03-30 | MSV000089167 | MassIVE

Quantitative proteomics identifies tumour matrisome signatures in patients with non-small cell lung cancer

Project description:The composition and remodelling of the extracellular matrix (ECM) are important factors in the development and progression of cancers, and the ECM is implicated in promoting tumour growth and restricting anti-tumour therapies through multiple mechanisms. The characterisation of differences in ECM composition between normal and diseased tissues may aid in identifying novel diagnostic markers, prognostic indicators and therapeutic targets for drug development. Using tissue from non-small cell lung cancer (NSCLC) patients undergoing curative intent surgery, we characterised quantitative tumour-specific ECM proteome signatures by mass spectrometry, identifying 161 matrisome proteins differentially regulated between tumour tissue and nearby non-malignant lung tissue. We defined a collagen hydroxylation functional protein network that is enriched in the lung tumour microenvironment. We validated two novel putative extracellular markers of NSCLC, the collagen cross-linking enzyme peroxidasin and a disintegrin and metalloproteinase with thrombospondin motifs 16 (ADAMTS16), for discrimination of malignant and non-malignant lung tissue. These proteins were up-regulated in lung tumour samples, and high PXDN and ADAMTS16 gene expression was associated with shorter survival of lung adenocarcinoma and squamous cell carcinoma patients, respectively. These data reveal tumour matrisome signatures in human NSCLC.

2023-06-16 | PXD041066 | Pride

CBX7 is a tumour suppressor that inhibits bladder cancer

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TET1 is a tumour suppressor that inhibits bladder cancer progression

Project description:TET1 is a tumour suppressor that inhibits bladder cancer progression

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The zingerone analog, acetyl zingerone, bolsters matrisome synthesis, inhibits MMPs, and represses IL-17A target gene expression

Project description:The zingerone analog, acetyl zingerone, bolsters matrisome synthesis, inhibits MMPs, and represses IL-17A target gene expression

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The zingerone analog, acetyl zingerone, bolsters matrisome synthesis, inhibits MMPs, and represses IL-17A target gene expression [Experiment 1]

Project description:The zingerone analog, acetyl zingerone, bolsters matrisome synthesis, inhibits MMPs, and represses IL-17A target gene expression [Experiment 1]

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The zingerone analog, acetyl zingerone, bolsters matrisome synthesis, inhibits MMPs, and represses IL-17A target gene expression [Experiment 2]

Project description:The zingerone analog, acetyl zingerone, bolsters matrisome synthesis, inhibits MMPs, and represses IL-17A target gene expression [Experiment 2]

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Neoplastic-stromal cell crosstalk regulates matrisome expression in pancreatic cancer

Project description:Purpose: The goal of this study was to identify BET-dependent pathways in the PDAC stroma and the epithelial compartment. Methods: Monocultures and Cocultures of a low passage PDAC cell line (MGH1319) and a cancer-associated fibroblast cell line (CAF-1) were treated with either BETi (CPI203) or CTRL for 24 hours. Each condition was done as a single experiment and all cells were subjected to FACS, RNA was isolated using the RNeasy Micro Kit (CAT No.74004) and sequenced at 75 bp Pair End on the NextSeq sequencer (Illumina). qRT–PCR validation was performed using TaqMan assays. Results: In vitro co-cultures of PDAC and CAF cells demonstrated that matrisome expression was regulated by BET-dependent PDAC-CAF crosstalk. Conclusions: PDAC matrisome expression is dependent on tumor-stroma crosstalk and regulated in parts by BET proteins.

2020-09-30 | GSE155442 | GEO

Manassantin A inhibits tumour growth under hypoxia through the activation of chaperone-mediated autophagy by modulating Hsp90 activity

Project description:Background: Chaperon-mediated autophagy (CMA) has taken on a new emphasis in cancer biology. However, the roles of CMA in hypoxic tumours are poorly understood. We investigated the anti-tumour effects of the natural product ManA through the activation of CMA in tumour progression under hypoxia. Methods: The effect of ManA on CMA activation was assessed in mouse xenograft models and cells. The gene expressions of HIF-1α, HSP90AA1, and transcription factor EB (TFEB) were analysed using The Cancer Genome Atlas (TCGA) datasets to assess the clinical relevance of CMA. Results: ManA activates photoswitchable CMA reporter activity and inhibits Hsp90 chaperone function by disrupting the Hsp90/F1F0-ATP synthase complex. Hsp90 inhibition enhances the interaction between CMA substrates and LAMP-2A and TFEB nuclear localisation, suggesting CMA activation by ManA. ManA-activated CMA retards tumour growth and displays cooperative anti-tumour activity with anti-PD-1 antibody. TCGA datasets show that a combined expression of HSP90AA1High/HIF1AHigh or TFEBLow/HIF1AHigh is strongly correlated with poor prognosis in patients with lung cancer. Conclusions: ManA-induced CMA activation by modulating Hsp90 under hypoxia induces HIF-1α degradation and reduces tumour growth. Thus, inducing CMA activity by targeting Hsp90 may be a promising therapeutic strategy against hypoxic tumours.

2024-01-22 | GSE110768 | GEO

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