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Separated Pancreatic stellate cells (PSCs) by functional separation using modified Matrigel invasion assay

ABSTRACT: We separated PSCs by functional separation using moidfied Matrigel invasion assay our previously reported (Fujiwara, PLoS One, 2012). In this culture system, we evaluated two primary cultures of human PSCs. PSCs in the upper chambers were incubated for 72 hours in culture with SUIT-2 pancreatic cancer cells in the lower chambers, or as controls without pancreatic cancer cells in the lower chambers, and were collected from the top and bottom sides of the upper chambers separately. The top side-derived PSCs were cells that did not migrate toward the cancer cells, and the bottom side-derived PSCs were cells that migrated toward the pancreatic cancer cells. We then performed a DNA microarray analysis using these cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE55300 | GEO | 2014/02/25

SECONDARY ACCESSION(S): PRJNA239243

REPOSITORIES: GEO

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Separated Pancreatic stellate cells (PSCs) by functional separation using modified Matrigel invasion assay

Project description:We separated PSCs by functional separation using moidfied Matrigel invasion assay our previously reported (Fujiwara, PLoS One, 2012). In this culture system, we evaluated two primary cultures of human PSCs. PSCs in the upper chambers were incubated for 72 hours in culture with SUIT-2 pancreatic cancer cells in the lower chambers, or as controls without pancreatic cancer cells in the lower chambers, and were collected from the top and bottom sides of the upper chambers separately. The top side-derived PSCs were cells that did not migrate toward the cancer cells, and the bottom side-derived PSCs were cells that migrated toward the pancreatic cancer cells. We then performed a DNA microarray analysis using these cells. The quality of the RNA samples was evaluated using Experion™ Automated Electrophoresis Station (Bio-Rad Laboratories, Hercules, CA). We used a HumanHT-12v4 Expression BeadChip (Illumina, San Diego, CA) for these analyses. The data were analyzed using Bead Studio software version 3.2.3 (Illumina).

2014-02-25 | E-GEOD-55300 | biostudies-arrayexpress

Analysis of RNA distribution between pseudopodia and cell bodies in response to Fibronectin

Project description:The goal of the study was to identify on a genome-wide scale RNAs that are enriched at the leading edge of migrating cells. For this, we employed a fractionation method in which cells are plated on a microporous filter whose bottom side only is coated with fibronectin. The cells thus polarize and extend pseudopodial protrusions towards the bottom surface. These protruding pseudopodia can then be physically isolated from the bottom surface of the filter and their contents compared with the remaining cell bodies, which are isolated from the upper surface of the filter. Keywords: comparative RNA distribution

2008-03-18 | GSE10227 | GEO

Characterisation and use of orthotopically grownHapT1tumours in its homologous host as a preclinical model to evaluate novel drugs against desmoplastic pancreatic cancer

Project description:The major objective of this study was to characterise theHapT1 orthotopic hamster pancreatic tumor as a preclinical model of desmoplastic pancreatic ductal adenocarcinoma; and use this model to validate the efficacy of drugs that kills activated pancreatic stellate cells (PSCs)in vitro. Experimentaldesign: Commercially procured HapT1 pancreatic cancer (PCA) cell line was implanted in the pancreas of its syngeneic host, Syrian golden hamster (Mesocricetusauratus). After certain time period the primary and secondary tumors were harvested for histological andimmunophynotypical analysis. PSCs of hamsters were harvested, cultured and characterised. The in-cultured activated rodent PSCs and commercially procured human PSCs were used to check the cytotoxic effect of Disulfiram (DSF) in presence and absence of copper (Cu )in vitro. Finally, theHapT1 orthotopic tumor model was used to check the efficacy of DSF in vivo.

2018-10-26 | PXD003385 | Pride

Transcription profiling of mouse migrating cell bodies vs pseudopodia fibronectin

2008-04-05 | E-GEOD-10227 | biostudies-arrayexpress

Analysis of RNA distribution between pseudopodia and cell bodies in response to LPA stimulation

Project description:The goal of the study was to identify on a genome-wide scale RNAs that are enriched at the leading edge of migrating cells. For this, we employed a fractionation method in which serum-starved cells are first plated and allowed to spread on a microporous filter. Addition of LPA at the bottom side of the filter induces the cells to polarize and extend pseudopodial protrusions. These protruding pseudopodia can then be physically isolated from the bottom surface of the filter and their contents compared with the remaining cell bodies, which are isolated from the upper surface of the filter. Keywords: comparative RNA distribution

2008-03-18 | GSE10226 | GEO

Role of Macrophage migration inhibitory factor (MIF) in pancreatic stellate cells (PSCs)

Project description:The presence of activated pancreatic stellate cells (PSCs) in the pancreatic ductal adenocarcinoma (PDAC) microenvironment plays a significant role in cancer progression. Macrophage migration inhibitory factor (MIF) is overexpressed in PDAC tissues and expressed by both cancer and stromal cells. The expression status of MIF and its receptors in PDAC- associated fibroblasts or PSCs and its pathophysiological roles are yet to be elucidated. The next-generation sequencing technique was adapted to check the effect of MIF absence on the expression of other genes in mice (mPSCs).

2022-09-28 | E-MTAB-9392 | biostudies-arrayexpress

Transcription profiling of mouse pseudopodia and cell bodies in response to LPA stimulation

Project description:The goal of the study was to identify on a genome-wide scale RNAs that are enriched at the leading edge of migrating cells. For this, we employed a fractionation method in which serum-starved cells are first plated and allowed to spread on a microporous filter. Addition of LPA at the bottom side of the filter induces the cells to polarize and extend pseudopodial protrusions. These protruding pseudopodia can then be physically isolated from the bottom surface of the filter and their contents compared with the remaining cell bodies, which are isolated from the upper surface of the filter. Experiment Overall Design: We analyzed two independent pseudopodia samples (05-61_PS_A and 06-04_PS_A) and two independent cell body samples (05-61_CB_A and 06-04_CB_A)

2008-04-05 | E-GEOD-10226 | biostudies-arrayexpress

Vitamin d receptor-mediated stromal reprogramming suppresses pancreatitis and enhances pancreatic cancer therapy

Project description:The poor clinical outcome in pancreatic ductal adenocarcinoma (PDA) has been attributed to intrinsic resistance to chemotherapy and a growth-permissive tumor microenvironment. Quiescent pancreatic stellate cells (PSCs) are neuroendocrine, nestin-positive, lipid-accumulating cells whose homologues in the liver are the principal repository of Vitamin A esters. Upon activation, lipid droplets are lost and via transdifferentiation they become the key cell type responsible for driving the severe desmoplasia that characterizes PDA. Despite their critical role in PDA progression and chemoresistance, therapeutic strategies targeting PSCs are lacking. Here we identified the vitamin D receptor (VDR) as a master genomic regulator of PSC activation and function. In vitro we demonstrate that VDR activation reduces expression in PSCs of genes implicated in activation, inflammation, and extracellular matrix production, as well as restoring lipid droplet integrity. In vivo, the VDR ligand calcipotriol enhances the anti-tumor effects of gemcitabine by increasing intratumoral concentration 5-fold, reducing tumor volume to near baseline and lowering metastases by more than 65%. These findings implicate VDR as a master regulator of PSC activation and identify a novel therapeutic approach for the treatment of pancreatic cancer. RNA-Seq analyses was used to characterize cancer-associated changes between pre-activated (3-day culture) and activated (7-day culture) primary mouse PSCs, as well as control and PDA human PSCs. RNA-Seq was also used to assess the impact of VDR activation (DMSO vs calcipotriol) in a human PSC line (MiaPaCa-2), the mouse primary PSCs

2014-10-03 | E-GEOD-43770 | biostudies-arrayexpress

ERAP2 is a novel target involved in autophagy and activation of pancreatic stellate cells via unfolded protein response signaling pathway

Project description:Pancreatic ductal adenocarcinoma (PDAC) is characterized by excessive desmoplasia and autophagy-dependent tumorigenic growth. Pancreatic stellate cells (PSCs) as a predominant stromal cell type play a critical role in PDAC biology. Autophagy facilitates PSC activation. However, the mechanism remains unknown. To investigate the mechanism of autophagy in PSC activation, gene expression profiles between patient-derived PSCs from pancreatic cancer and chronic pancreatitis were compared using a gene expression microarray. Here, we found that endoplasmic reticulum aminopeptidase 2 (ERAP2), which resides in the endoplasmic reticulum (ER) membrane, was highly expressed in both cancer-associated PSCs and pancreatic cancer cells (PCCs). We found that high stromal ERAP2 expression is associated with a poor prognosis of PDAC patients. Knockdown of ERAP2 inhibited autophagy of PSCs and PCCs. In PSCs, inhibition of autophagy by ERAP2 knockdown led to inactivation of PSCs and attenuated tumor-stromal interactions. This process was mediated by ER stress and consequent IRE1α and PERK unfolded protein response (UPR) signaling pathways. In orthotopic models, ERAP2 knockdown in PSCs inhibited growth and fibrosis of xenografted tumor compared with coimplantation of PSCs without ERAP2 knockdown, and gemcitabine treatment further inhibited tumor growth. Our findings demonstrate a novel mechanism of PSCs activation regulated by autophagy. ERAP2 as a promising therapeutic target may provide a novel strategy for the treatment of PDAC.

2022-04-30 | GSE172168 | GEO

Colorectal cancer initiation site

Project description:The role of stem cells in solid tumors remains controversial. In colorectal cancers (CRC), this is complicated by the conflicting ‘top-down’ or ‘bottom-up’ hypothesis of cancer initiation. We profiled the expressions of genes from the top (T) and bottom (B) fractions of the crypt in morphologically normal-appearing colonic mucosa (M) and contrasted this to that of matched mucosa adjacent to tumors (MT) in twenty three sporadic CRC patients. In thirteen patients, the genetic distance (M-MT) between the B fractions is smaller than the distance between the T fractions indicating that the expressions of significant genes diverge further in the top fractions (B<T). In the remaining ten patients, the reverse is observed (B>T). Taking genetic divergence as an intermediate endpoint, the data indicates that it is equally likely that CRC initiates from ‘top-down’ via dedifferentiated colonocytes or ‘bottom-up’ via dysregulated intestinal stem cells. This has important ramification for subsequent therapeutic considerations.

2018-06-18 | GSE97689 | GEO

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