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Cell-derived extracellular matrix (CDM) from human pancreatic ductal cells (HPDE)

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is characterised by an abundant desmoplastic reaction which includes an excess production of extracellular matrix. The extracellular matrix produced by HPDE cells (H6c7), with and without expression of mutant KRas G12V, was analysed by LC-MSMS

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

DISEASE(S): Pancreatic Cancer

SUBMITTER: Jon Humphries

LAB HEAD: Martin J Humphries

PROVIDER: PXD027803 | Pride | 2022-05-20

REPOSITORIES: Pride

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Pancreatic ductal adenocarcinoma cells employ integrin α6β4 to form hemidesmosomes and regulate cell proliferation.

Humphries Jonathan D JD Zha Junzhe J Burns Jessica J Askari Janet A JA Below Christopher R CR Chastney Megan R MR Jones Matthew C MC Mironov Aleksandr A Knight David D O'Reilly Derek A DA Dunne Mark J MJ Garrod David R DR Jorgensen Claus C Humphries Martin J MJ

Matrix biology : journal of the International Society for Matrix Biology 20220409

Pancreatic ductal adenocarcinoma (PDAC) has a dismal prognosis due to its aggressive progression, late detection and lack of druggable driver mutations, which often combine to result in unsuitability for surgical intervention. Together with activating mutations of the small GTPase KRas, which are found in over 90% of PDAC tumours, a contributory factor for PDAC tumour progression is formation of a rigid extracellular matrix (ECM) and associated desmoplasia. This response leads to aberrant integr ...[more]

PMID: 35405272

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Integrin adhesion complex (IAC) analysis from human pancreatic ductal cells (HPDE)

Project description:Pancreatic ductal adenocarcinoma (PDAC) is characterised by an abundant desmoplastic reaction which includes an excess production of extracellular matrix and interacts with integrin adhesion receptors. Integrin adhesion complexes formed by HPDE cells (H6c7), with and without expression of mutant KRas G12V, were isolated and analysed by LC-MSMS

2022-05-20 | PXD027827 | Pride

Proteomic analysis of healthy and hyperglycemic murine fetal kidneys

Project description:Alteration of kidney morphogenesis in diabetic pregnancies is poorly described, especially changes in the extracellular matrix (ECM) and glomerular basement membrane (GBM during glomerulogenesis. Addressing the ECM proteome, or matrisome, in the mouse fetal kidney in a healthy and diabetic environment will improve understanding about the association between ECM changes in the kidney as potential reprogramming mechanisms of kidney differentiation in diabetic pregnancies. Therefore, to better understand ECM composition and remodelling in kidney developmental and appreciate the alterations associated to the maternal diabetes, this project aimed to define the matrisome in the mouse fetal kidney on embryonic day 19. For this, we used an ECM enrichment approach combined with high resolution label-free tandem mass spectrometry to define the matrisome in the fetal mouse kidney (healthy and hyperglycemic) to test the hypothesis that maternal diabetes influences ECM composition, assembly and, therefore, biology.

2021-10-13 | PXD025874 | Pride

Secretome from human pancreatic ductal cells (HPDE)

Project description:Pancreatic ductal adenocarcinoma (PDAC) is characterised by an abundant desmoplastic reaction which includes an excess production of extracellular matrix. The proteins and extracellular matrix secreted by HPDE cells (H6c7), with and without expression of mutant KRas G12V, was analysed by LC-MSMS

2022-05-20 | PXD027823 | Pride

Super-Enhancer-mediated Control of Liver Fibrosis by BET Bromodomain Proteins

Project description:Here, we investigate the role of enhancers in myofibroblasts, a cell type that dominates the pathogenesis and progression of tissue fibrosis. We reveal that bromodomain and extra-terminal family members (BETs), an important group of epigenetic readers, are critical for super-enhancer-mediated pro-fibrotic gene expression in hepatic stellate cells (HSCs, lipid-containing liver-specific pericytes), upon activation during liver fibrogenesis give rise to myofibroblasts2-4. We observe significantly enriched localization of BETs to hundreds of super-enhancers associated with genes involved in multiple pro-fibrotic pathways. This unique loading pattern consequentially serves as a molecular mechanism by which BETs modulate pro-fibrotic gene expression in myofibroblasts. Strikingly, suppression of BET-enhancer interaction using small-molecule inhibitors such as JQ1 dramatically blocks activation of HSCs into myofibroblasts and significantly compromises the proliferation of activated HSCs. Identification of BRD2, BRD3, BRD4, PolII, PolIIs2p and PolIIs5p binding sites in human stellate LX2 cells that were treated with DMSO (0.1%) or JQ1 (500nM) for 16 hrs.

2015-12-11 | E-GEOD-58680 | biostudies-arrayexpress

A master cistromic circuit governing hepatic fibrogenesis [ChIP-seq]

Project description:Liver fibrosis is a reversible wound-healing response to liver injury and hepatic stellate cells (HSCs) are central cellular players that mediate hepatic fibrogenesis. However, the molecular mechanisms that govern this process remain unclear. Here, we reveal a novel cistromic circuit in HSCs comprising the vitamin D receptor (VDR) and SMAD transcription factors that restrains the intensity of hepatic fibrogenesis. Ligand-activated VDR suppresses TGFβ1-induced pro-fibrotic gene expression in HSCs. Administration of a vitamin D analogue, calcipotriol, diminishes the fibrotic response in a mouse model of liver fibrosis, while VDR knockout mice spontaneous develop extensive hepatic fibrosis by age 6 months. Using ChIP-Seq, we find that the anti-fibrotic properties of VDR are due to crosstalk with SMAD, mediated by their co-occupancy of DNA-binding sites on pro-fibrotic genes. Specifically, SMAD binding potentiates local chromatin accessibility to enhance VDR recruitment at the same cis-regulatory elements, which reciprocally antagonizes the interaction between SMAD3 and chromatin and limits the assembly of transcriptional activation complexes at fibrotic genes, a process that is enhanced by the presence of VDR agonists. These results not only establish this coordinated VDR/SMAD cistromic circuit as a master regulator of hepatic fibrogenesis, but also support VDR as a potential drug target to ameliorate liver fibrosis. Identification of VDR, SMAD3 and H3 binding sites in human stellate LX2 cells that were pre-treated with calcipotriol (100nM) for 16 hrs (where calcipotriol treatment is indicated) followed by incubation of calcipotriol (100nM) or TGFβ1 (1ng/ml) for another 4 hours (where indicated).

2013-04-29 | E-GEOD-38103 | biostudies-arrayexpress

A Master Cistromic Circuit Governing Hepatic Fibrogenesis

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-04-29 | E-GEOD-41580 | biostudies-arrayexpress

Transcription profiling of human mammary epithelial cell lines with finite life span and immortal non-malignant cells - time series

Project description:Nonmalignant human mammary epithelial cells (HMEC) seeded in laminin-rich extracellular matrix (lrECM) form polarized acini and, in doing so, transit from a disorganized proliferating state to an organized growth-arrested state. We hypothesized that the gene expression pattern of organized and growth-arrested HMECs would share similarities with breast tumors with good prognoses. Using Affymetrix HG-U133A microarrays, we analyzed the expression of 22,283 gene transcripts in 184 (finite life span) and HMT3522 S1 (immortal nonmalignant) HMECs on successive days after seeding in a lrECM assay. Both HMECs underwent growth arrest in G0-G1 and differentiated into polarized acini between days 5 and 7. We identified gene expression changes with the same temporal pattern in both lines and examined the expression of these genes in a previously published panel of microarray data for 295 breast cancer samples. We show that genes that are significantly lower in the organized, growth-arrested HMEC than in their proliferating counterparts can be used to classify breast cancer patients into poor and good prognosis groups with high accuracy. This study represents a novel unsupervised approach to identifying breast cancer markers that may be of use clinically. Experiment Overall Design: We analyzed gene expression in 184 (finite life span) and HMT3522 S1 (immortal non-malignant) HMECs on successive days (3, 5, and 7) post-seeding in a laminin-rich extracellular matrix assay. Both HMECs underwent growth arrest in G0/G1 and differentiated into polarized acini between days 5 and 7.

2008-06-15 | E-GEOD-8096 | biostudies-arrayexpress

Transcription profiling time series of finite life span and immortal non-malignant human mammary epithelial cell lines

Project description:We analyzed gene expression in 184 (finite life span) and HMT3522 S1 (immortal non-malignant) HMECs on successive days (3, 5, and 7) post-seeding in a laminin-rich extracellular matrix assay. Both HMECs underwent growth arrest in G0/G1 and differentiated into polarized acini between days 5 and 7.

2007-03-15 | E-MEXP-1006 | biostudies-arrayexpress

Gene expression profiles of Ras mutants.

Project description:Gene expression profiles were collected from HEK-HT cells expressing H-Ras with Ras-activating (G12V), Raf-activating (G12V,T35S), RalGEF-activating (G12V,E37G), or PI3K-activating (G12V,Y40C) mutations. Keywords: Comparison of Ras pathway components. THX=control; 12V=G12V mutation; 35S=G12V,T35S mutation; 37G=G12V,E37G mutation; 40C=G12V,Y40C mutation. 5 replicates of each. Total of 25 samples.

2009-02-21 | E-GEOD-14934 | biostudies-arrayexpress

Gene expression profiles of Ras mutants.

2009-02-21 | GSE14934 | GEO

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