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Gene expression profiling of pancreatic cancer cell line BxPC-3 induced by PAR-2 AP

ABSTRACT: Protease-activated receptor-2 (PAR-2), a G protein-coupled receptor activated by trypsin and coagulant factors, plays broad spectrum of physiological and pathological roles especially in cancer development. In this study, we used PAR-2 activating peptide to mimic the action of trypsin to trigger PAR-2 signaling pathway and effects of PAR-2 activation on gene expression in human pancreatic cancer cell line BxPC-3 investigated by microarray analysis. Through DAVID bioinformatic resources, we observed that activated PAR-2-mediated genes are summarized to two different pathways, renal cell carcinoma and NFkB pathway. In renal cell carcinoma pathway, activated PAR-2 dysregulated hypoxia-inducible factors and its target genes, including glucose transporter 1 (GLUT1), transforming growth factor-b (TGF-b) and vascular endothelial growth factor-A (VEGF-A). In addition, activated PAR-2 induced MAPK signaling and transcriptional factors, such as JUN, MAP2K1 and ETS1. The regulation of these genes by PAR-2 assumed that PAR-2 signaling was associated with cancer progression. On the other hand, activated PAR-2 upregulated interleukin-1b (IL-1b) and toll-like receptor 4 (TLR4) related with NFkB activation, which indicated that PAR-2 signaling may cause cancer-related inflammation. In conclusion, PAR-2 may be a factor to regulate cancer progression and inflammation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE44827 | GEO | 2013/04/30

SECONDARY ACCESSION(S): PRJNA192255

REPOSITORIES: GEO

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Gene expression profiling of pancreatic cancer cell line BxPC-3 induced by PAR-2 AP

Project description:Protease-activated receptor-2 (PAR-2), a G protein-coupled receptor activated by trypsin and coagulant factors, plays broad spectrum of physiological and pathological roles especially in cancer development. In this study, we used PAR-2 activating peptide to mimic the action of trypsin to trigger PAR-2 signaling pathway and effects of PAR-2 activation on gene expression in human pancreatic cancer cell line BxPC-3 investigated by microarray analysis. Through DAVID bioinformatic resources, we observed that activated PAR-2-mediated genes are summarized to two different pathways, renal cell carcinoma and NFkB pathway. In renal cell carcinoma pathway, activated PAR-2 dysregulated hypoxia-inducible factors and its target genes, including glucose transporter 1 (GLUT1), transforming growth factor-b (TGF-b) and vascular endothelial growth factor-A (VEGF-A). In addition, activated PAR-2 induced MAPK signaling and transcriptional factors, such as JUN, MAP2K1 and ETS1. The regulation of these genes by PAR-2 assumed that PAR-2 signaling was associated with cancer progression. On the other hand, activated PAR-2 upregulated interleukin-1b (IL-1b) and toll-like receptor 4 (TLR4) related with NFkB activation, which indicated that PAR-2 signaling may cause cancer-related inflammation. In conclusion, PAR-2 may be a factor to regulate cancer progression and inflammation. Two-condition experiment, control cells vs PAR-2 AP-treated cells.

2013-04-30 | E-GEOD-44827 | biostudies-arrayexpress

Human prostate carcinoma cell line 22Rv1 overexpressing ESE1

Project description:Activation of the inflammatory circuits occurs frequently in cancer cells. However the molecular details linking inflammation to transformation and progression are still unknown. In this study we report for the first time, that activation of the ETS factor ESE1 is a key event connecting inflammatory signaling with prostate cancer progression. We report that ESE1 is induced upon IL-1 beta stimulation by NFKB and mediates key transcriptional changes involving cell adhesion, migration and invasion. ESE1 activation in turn induces NFKB transcriptional activation and intranuclear translocation and mediates the transforming phenotypes linked to the activation of IL-1B. Transcriptional signatures and immunohistochemistry revealed that this ESE1-NFKB regulatory circuit also operates in prostate tumors, particularly in those with significant elevation of ESE1. Thus, ESE1 promotes an inflammatory feed forward loop positively leading to prostate cancer progression. Pharmacological NFKB inhibition reverted the transformed status of ESE1 cell lines providing a rationale for context-dependent therapeutic strategies in ESE1 activated tumors. These studies find a previously unrecognized link between ETS and activation of the NFKB pathway and open new avenues for prostate cancer treatment. Gene expression analysis of a control cell line (22Rv1-pcDNA3.1) and a testing cell lines (22Rv1-ESE1), with two replicates, with dye swap, performed for each sample.

2013-06-20 | E-GEOD-39668 | biostudies-arrayexpress

Human prostate carcinoma cell line 22Rv1 overexpressing ESE1

2013-06-20 | GSE39668 | GEO

The Mutational Landscape of CTCL and Sezary Syndrome.

Project description:<p>Sezary syndrome is a leukemic and aggressive form of cutaneous T-cell lymphoma (CTCL) resulting from the malignant transformation of skin-homing central memory CD4+ T cells. To identify new genetic alterations involved in Sezary syndrome and CTCL transformation we performed whole-exome sequencing of tumor-normal sample pairs from 26 Sezary syndrome and 16 CTCL patients. These analyses revealed a distinctive pattern of somatic copy number alterations in Sezary syndrome including highly prevalent recurrent chromosomal deletions involving the TP53, RB1, PTEN, DNMT3A, and CDKN1B tumor suppressor genes. Mutation analysis identified a broad spectrum of somatic mutations involving key genes involved in epigenetic regulation (TET2, CREBBP, MLL3, BRD9, SMARCA4 and CHD3) and signaling, including mutations in MAPK1, BRAF, CARD11 and PRKG1 driving increased MAPK, NFKB and NFAT activity upon T-cell receptor stimulation. Collectively, our findings provide new insights into the genetics of Sezary syndrome and CTCL and support the development of personalized therapies targeting key oncogenically activated signaling pathways for the treatment of these diseases.</p>

| phs000994 | dbGaP

Transcription profiling of rat thrombin-stimulated vascular smooth muscle cells

Project description:The strength and duration of extracellular signal-regulated kinases 1/2 (ERK1/2) phosphorylation can define the phenotypic outcome of cells. Stimualtion of the proteinase-activated receptor (Par) triggers a Gi-dependent long-lasting transactivation of the epidermal growth factor receptor and subsequent ERK1/2 phosphorylation. To understand the mechnaisms underlying this signaling cascade, microarray analysis was performed in vascular smooth muscle cells. Experiment Overall Design: Par receptors on neonatal rat aortic smooth muscle cells were stimulated with thrombin or TRAP in presence or abscence of Gi-uncoupling pertussis toxin.

2009-05-02 | E-GEOD-15841 | biostudies-arrayexpress

Homo sapiens

Project description:Protease activated receptor 2 (PAR2) on HEK293 activated by trypsin or 2f-LIGRLO-NH2

| PRJNA132745 | ENA

Genome-wide analysis of short-term transcriptional responses in thrombin-stimulated vascular smooth muscle cells

2009-04-28 | GSE15841 | GEO

Cancer -associated mutations in XPO1 transform cells through altered nuclear export signal recognition

Project description:Proper nucleocytoplasmic distribution of proteins is essential to cellular homeostasis but what role the altered nuclear export machinery commonly described in cancer cells plays in cancer initiation is not known. Here, genomic analysis of 42,793 cancers identified recurrent mutational hotspots in XPO1, the main nuclear export receptor in eukaryotic cells. Expression of XPO1 mutations in vivo was sufficient to initiate clonal, B-lymphoproliferative disorders by altering the constellation of proteins exported from the nucleus based on amino acid charge C-terminal to their nuclear export signal. Impaired export of one such protein, the NFkB inhibitor IB enhanced NFkB signaling, a pathway frequently activated by somatic mutations in cancers enriched in XPO1 mutations. These data identify change-of-function mutations in nuclear export as novel drivers of tumorigenesis.

2021-09-01 | GSE120231 | GEO

Human platelet detergent resistant membranes proteome

Project description:Here we characterized the proteins associated with detergent resistant membranes (DRMs) from resting and activated human platelets. We achieved a proteomic profile of 141 DRM proteins involved in many biological pathways including 'PAR-1-mediated thrombin signal events', 'Integrin family cell surface interactions', 'Platelet activation, signalling and aggregation' and 'Platelet degranulation'. Therefore, a high level of relevant platelet signalling and trafficking proteins were identified e.g., Rap 1b, Src, SNAP-23 and syntaxin-11, implicating platelet DRMs as concentrating platforms not only in the critical platelet function of activation but also in secretion/degranulation.

2016-06-23 | PXD002554 | Pride

To identify the deficient enzyme(s) in the glycosylation pathway that yield incomplete maturation of (uPAR) protein

Project description:We previously demonstrated plasticity in urokinase receptor (u-PAR) display in clonal colon cancer cells (Cancer Research 66: 7957-7967 (2006)). Thus, u-PAR display oscillates 10 fold between high and low density at the cell surface. We have determined that this oscillation in u-PAR display is posttranslational in nature. Thus, while clonal cell populations with high and low u-PAR density synthesize u-PAR at the same rate, the protein is inefficiently glycosylated in cells down-shifted for u-PAR display and subsequently degraded.

2011-09-06 | GSE31929 | GEO

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