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Senescent lung fibroblasts in idiopathic pulmonary fibrosis facilitate non-small cell lung cancer progression by secreting exosomal MMP1

ABSTRACT: Senescent lung fibroblasts in idiopathic pulmonary fibrosis facilitate non-small cell lung cancer progression by secreting exosomal MMP1

PROVIDER: PRJNA1173747 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31017114_1.fastq.gz	Fastqsanger.gz
	SRR31017114_2.fastq.gz	Fastqsanger.gz
	SRR31017115_1.fastq.gz	Fastqsanger.gz
	SRR31017115_2.fastq.gz	Fastqsanger.gz
	SRR31017116_1.fastq.gz	Fastqsanger.gz

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Senescent lung fibroblasts in idiopathic pulmonary fibrosis facilitate non-small cell lung cancer progression by secreting exosomal MMP1

Project description:Lung cancer is a fatal complication of idiopathic pulmonary fibrosis (IPF) with a poor prognosis. Current treatments are insufficient in improving the prognosis of lung cancer patients with comorbid idiopathic pulmonary fibrosis (IPF-LC). Senescent fibroblasts play a pivotal role within the tumor microenvironment, influencing tumor progression by secreted exosomes. With evidence that fibroblast senescence is an important mechanism of IPF, we sought to investigate the impact of senescent IPF lung fibroblast-derived exosomes on non-small cell lung cancer (NSCLC). Our results show that IPF fibroblasts (diseased human lung fibroblasts, DHLF) express significant senescence markers, promoting NSCLC proliferation, invasion, and epithelial-mesenchymal transition. Specifically, we observed senescent DHLFs secret more exosomes (DHLF-exosomes), which could enhance proliferation and colony-forming ability of cancer cells. Proteomic analysis of DHLF-exosomes identified upregulation of SASP factors, notably MMP1, which activates the surface receptor PAR1. Knocking down MMP1 or using PAR1 inhibitors reduced the tumor-promoting effects of DHLF-exosomes in vivo and in vitro. Mechanistically, MMP1 acted via activating the PI3K-AKT-mTOR pathway. In conclusion, our results suggest that exosomal MMP1 derived from senescent IPF fibroblasts promotes NSCLC proliferation and colony formation by targeting PAR1 and activating the PI3K-AKT-mTOR pathway. These findings provide a novel therapeutic approach for patients with IPF-LC.

2024-10-21 | GSE279637 | GEO

Senescent lung fibroblasts in idiopathic pulmonary fibrosis facilitate non-small cell lung cancer progression by secreting exosomal MMP1.

Project description: Not available

| S-EPMC11888990 | biostudies-literature

MMP1 and MMP7 as potential peripheral blood biomarkers in Idiopathic Pulmonary Fibrosis

Project description:Idiopathic pulmonary fibrosis (IPF) is a chronic progressive fibrotic lung disease associated with significant morbidity and mortality. We identified a combinatorial signature of 5 proteins that was sufficient to distinguish IPF patients from controls; of these proteins MMP7 and MMP1 exhibited significantly higher values in both peripheral blood concentrations and lung tissue gene expression, suggesting their role as true biomarkers. Keywords: disease versus control

2009-02-20 | GSE10667 | GEO

Development of diagnostic exosomal biomarkers for the detection of invasive non-functional pituitary adenomas (NFPAs)

Project description:The incomplete surgical resection of invasive non-functional pituitary adenomas (iNFPAs) carries the increased risk of complications and requires adjuvant radiotherapy and medications. Thus, the molecular mechanisms and markers of invasiveness must be identified to guide the management of NFPA patients. This study explores the proteomic and transcriptomic variations of invasive and non-invasive NFPAs and other types of pituitary adenomas and evaluates the genetic markers in the exosome related to iNFPAs. The exosome from invasive and non-invasive NFPAs, prolactinomas (PRLs), growth hormone–secreting adenomas (GHs), adrenocorticotropic hormone-secreting adenomas (ACTHs), and normal pituitary tissue were analyzed. We confirmed that elevated matrix metalloproteinase-1 (MMP1) expression and its production in the exosome (exo-MMP1) are correlated with the invasive characteristics of NFPA. To investigate the molecular mechanism underlying the role of exo-MMP1 in invasiveness, we analyzed the effects of MMP1 on cell migration, cell growth and tumor angiogenesis. After transfection of MMP1 or a shRNA expression vector into NFPA cells, we obtained the associated exosome and observed that the altered expression and production of MMP1 in the exosome was significantly synchronized with the transduction of NFPA cells. In addition, the enrichment of MMP1 in the exosome promoted cell migration, cell growth and tumor angiogenesis via protease-activated receptor-1 (PAR1) signaling in recipient cells. Thus, these data demonstrate that MMP1 plays an important role in tumor invasion and angiogenesis and show that an exosome-mediated regulatory pathway for MMP1 may represent a target for therapeutic treatment.

2016-11-12 | GSE89779 | GEO

Staphylococcus warneri strain:MMP1

Project description:Staphylococcus warneri strain:MMP1 Genome sequencing and assembly

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Human peripheral IL-10-secreting vs non- IL-10-secreting B cells

Project description:Transcriptional profiling of human peripheral B cell subsets sorted by flow cytometry based on the secretion of IL-10 in response to CpG2006 stimulation. Goal was to identify molecular markers to distinguish IL-10-producing B cells form non-IL-10-producing B cells. Two-condition experiment, non-IL-10-secreting B cells vs. IL-10-secreting B cells. Healthy donors. Biological replicates: 6

2013-03-04 | E-GEOD-35002 | biostudies-arrayexpress

A Pvr–AP-1–Mmp1 signaling pathway is activated in astrocytes upon traumatic brain injury

Project description:Traumatic brain injury (TBI) caused by external mechanical forces is a major health burden worldwide, but the underlying mechanism in glia remains largely unclear. We report herein that Drosophila adults exhibit a defective blood-brain-barrier (BBB), elevated innate immune responses, and appear to be hypertrophy of astrocytes upon consecutive strikes with a high-impact trauma device. RNA sequencing (RNA-seq) analysis of these astrocytes revealed upregulated expression of genes encoding PDGF and VEGF receptor-related (Pvr, a receptor tyrosine kinase (RTK)), adaptor protein complex 1 (AP-1, a transcription factor complex of the c-Jun N-terminal Kinase (JNK) pathway) composed of Jun-related antigen (Jra) and kayak (kay), and matrix metalloproteinase 1 (Mmp1) following TBI. Interestingly, Pvr is both required and sufficient for AP-1 and Mmp1 upregulation, while knockdown of AP-1 expression in the background of Pvr overexpression in astrocytes rescued Mmp1 upregulation upon TBI, indicating that Pvr acts as the upstream receptor for the downstream AP-1–Mmp1 transduction. Moreover, dynamin-associated endocytosis was found to be an important regulatory step in downregulating Pvr signaling. Our results identify a new Pvr–AP-1–Mmp1 signaling pathway in astrocytes in response to TBI, providing potential targets for developing new therapeutic strategies of TBI.

2024-06-30 | GSE263447 | GEO

Prolyl hydroxylase P4HA1 is amplified, overexpressed in prostate cancer and enhances cancer invasion by altering MMP1 expression

Project description:Recent studies including next-generation sequencing have identified genomic events in prostate cancer including ETS gene fusions. However, it is critical to identify druggable targets for prostate cancer and their mechanism of action for therapeutic intervention. Here, we show that prolyl 4-hydroxylase, alpha polypeptide I (P4HA1) is overexpressed in aggressive prostate cancer and amplified in a subset of metastatic prostate cancer. This study provides mechanistic insights of P4HA1 regulation and its mode of action including its role in regulating MMP1. Importantly, P4HA1 mediated invasion in cancer cells could be reversed using MMP1 inhibitor, revealing therapeutic utility of targeting P4HA1 either directly or by inhibiting its downstream effectors. Two-color experiment, in duplicates.

2015-05-10 | E-GEOD-55787 | biostudies-arrayexpress

Modeling Molecular Pathogenesis of Idiopathic Pulmonary Fibrosis-Associated Lung Cancer in Mice

Project description:Idiopathic Pulmonary Fibrosis (IPF) is characterized by progressive, often fatal loss of lung function due to overactive collagen production and tissue scarring. IPF patients have a sevenfold-increased risk of developing lung cancer. The COVID-19 pandemic has increased the number of patients with lung diseases, and infection can worsen prognoses for those with chronic lung diseases and disease-associated cancer. Understanding the molecular pathogenesis of IPFassociated lung cancer is imperative for identifying diagnostic biomarkers and targeted therapies that will facilitate prevention of IPF and progression to lung cancer. To understand how IPF-associated fibroblast activation, matrix remodeling, epithelial-mesenchymal transition, and immune modulation influences lung cancer predisposition, we developed a mouse model to recapitulate the molecular pathogenesis of pulmonary fibrosis-associated lung cancer using the bleomycin and Lewis Lung Carcinoma models. We demonstrate that development of pulmonary fibrosis-associated lung cancer is likely linked to increased abundance of tumor-associated macrophages and a unique gene signature that supports an immune-suppressive microenvironment through secreted factors. Not surprisingly, pre-existing fibrosis provides a pre-metastatic niche and results in augmented tumor growth, and tumors associated with bleomycin-induced fibrosis are characterized by a dramatic loss of cytokeratin expression, indicative of epithelial-to-mesenchymal transition. Implications: This characterization of tumors associated with lung diseases provides new therapeutic targets that may aid in the development of treatment paradigms for lung cancer patients with pre-existing pulmonary diseases.

2023-06-20 | GSE224134 | GEO

Prolyl hydroxylase P4HA1 is amplified, overexpressed in prostate cancer and enhances cancer invasion by altering MMP1 expression

2015-05-10 | GSE55787 | GEO