Ontology highlight
ABSTRACT:
PROVIDER: PRJNA345216 | ENA |
REPOSITORIES: ENA
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Project description:Hepatic Deletion of Janus Kinase 2 Counteracts Inflammation, Oxidative Stress and Liver Cancer Formation in Growth Hormone Transgenic Mice
2017-10-11 | E-MTAB-3774 | ExpressionAtlas
Project description:Neutrophil oxidative stress mediates obesity-associated vascular inflammation and metastatic transmigration
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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
Project description:Benign prostatic hyperplasia and related lower urinary tract symptoms remain common, costly, and impactful issues for aging males. Etiology and pathogenesis are multifactorial and include steroid hormone changes and inflammation. Noninvasive markers could one day inform personalized medicine, but interindividual variation and lack of healthy age-matched controls hamper research. Experimental models are appealing for insight into disease mechanisms. Here, we present a spatiotemporal proteomics study in a mouse model of hormone-induced urinary dysfunction. Urine samples were collected noninvasively across time: before, during, and after disease onset. Microcomputed tomography analysis implicated the prostate as a spatially relevant contributor to bladder outlet obstruction. Prostates were collected after disease onset and compared with control mice. Notable changes in urine include proteins representing oxidative stress defense and acute phase inflammatory response processes. In the prostate, hormone treatment led to perturbations related to oxidative stress response and H2O2 metabolism. Several protein changes coincided in both urine and prostate tissue, including Ctsb, Qsox1, and Gpx3. This study supports the concept of noninvasive urinary biomarkers for prostate disease diagnostics. Oxidative stress and acute phase inflammatory processes were identified as key consequences of hormone-induced bladder outlet obstruction. Future research into antioxidants and anti-inflammatories in prostate disease appears promising.
2021-09-08 | PXD014416 | Pride
Project description:Insights into the mechanism of cell death induced by saporin delivered into cancer cells by an antibody fusion protein targeting the transferrin receptor 1 These studies detail transcriptional changes induced in cancer cells by the complex of saporin (b-SO6) and the antibody fusion protein ch128.1Av. Delivery of saporin into cancer cells by ch128.1Av, induces a transcriptional response consistent with oxidative stress and DNA damage, a response that is not observed with ch128.1Av alone. Time course, after delivery of saporin into cells by ch128.1Av
2012-11-09 | E-GEOD-42138 | biostudies-arrayexpress
Project description:Key histological and growth progression characteristics of human prostate cancer are phenocopied in mouse models that have been subjected to androgen level depletion and engineered for hemizygosity of candidate prostate cancer tumor suppressor genes Nkx3.1 and Pten. To characterize their relative transcriptomes and identify a genomic basis for their relevance to human prostate cancers, we compared mouse prostate tumors expression profiles to those from a panel of human prostate cancer isolates and to normal and benign prostates. Human prostate cancers and mouse prostate tumor models both exhibit the activation of genes associated with growth, cell cycle control, and inhibition of differentiation (CDKN2A, CDKN2B, CDKN2C, CEBPB, CEBPG, CSF1, CTSS, DMBT1, EGFR, PLCG2, PXN, SPP1, TNFSF9), and conversely, diminished expression of genes associated with normal prostate differentiation and function. All tumors also exhibit dysregulated expression of genes associated with inflammation, the disruption of prostate-associated ER stress pathways, as well as with oxidative stress, energy metabolism, cell adhesion, and stress response. Immunoinflammatory and altered cell adhesion process-associated genes exhibited prominent expression in early stage tumors. In contrast, metastatic human prostate cancer samples eliminated the expression of most immunoinflammatory-associated transcripts. Cross-species comparisons of molecular programs that are shared or distinguishing of Nkx3.1; Pten mutant mouse models and human adenocarcinomas clearly delineate core tumorigenesis programs associated with cell cycle activation and loss of differentiation. Compared to locally spreading mouse and human tumors, metastatic prostate cancer exhibits greatly reduced expression of immunoinflammatory and adhesion genes, implying that immuno-inflammatory activation may enable first stages of tumorogenesis, but suppress metastasis. These results provide a novel framework to identify stage-specific biomarkers and candidate targets for combinatorial therapeutics. The complex role of inflammation suggests a need for additional caution in countering metastasis. Keywords: tumor stage 26 Affymetrix MOE430A microarrays
2009-10-31 | E-GEOD-15943 | biostudies-arrayexpress
Project description:The epidemiologic association between statin use and decreased risk of advanced prostate cancer suggests that statins may inhibit prostate cancer development and/or progression. Studies were performed to determine the effects of a model statin, atorvastatin (ATO), on the proliferation and differentiation of prostate cancer cells, and to identify possible mechanisms of ATO action. ATO inhibited the in vitro proliferation of both LNCaP and PC3 human prostate cancer cells in dose-dependent fashion. The greater inhibitory activity of ATO in PC3 cells was associated with induction of autophagy in that cell line, as demonstrated by increased expression of LC3-II. miR-182 was consistently upregulated by ATO in PC3 cells, but not in LNCaP cells. ATO upregulation of miR-182 in PC3 cells was p53-independent and was reversed by geranylgeraniol. Transfection of miR-182 inhibitors decreased expression of miR-182 by >98% and attenuated the antiproliferative activity of ATO. miR-182 expression in PC3 cells was also increased in response to stress induced by serum withdrawal, suggesting that miR-182 upregulation can occur due to nutritional stress. Bcl2 and p21 were identified to be potential target genes of miR-182 in PC3 cells. Bcl2 was downregulated and p21 was upregulated in PC3 cells exposed to ATO. These data suggest that miR-182 may be a stress-responsive miRNA that mediates ATO action in prostate cancer cells. Gene and miRNA expression in two prostate cancer cell lines treated with Atorvastatin vs. untreated control.
2013-09-30 | E-GEOD-46375 | biostudies-arrayexpress
Project description:The epidemiologic association between statin use and decreased risk of advanced prostate cancer suggests that statins may inhibit prostate cancer development and/or progression. Studies were performed to determine the effects of a model statin, atorvastatin (ATO), on the proliferation and differentiation of prostate cancer cells, and to identify possible mechanisms of ATO action. ATO inhibited the in vitro proliferation of both LNCaP and PC3 human prostate cancer cells in dose-dependent fashion. The greater inhibitory activity of ATO in PC3 cells was associated with induction of autophagy in that cell line, as demonstrated by increased expression of LC3-II. miR-182 was consistently upregulated by ATO in PC3 cells, but not in LNCaP cells. ATO upregulation of miR-182 in PC3 cells was p53-independent and was reversed by geranylgeraniol. Transfection of miR-182 inhibitors decreased expression of miR-182 by >98% and attenuated the antiproliferative activity of ATO. miR-182 expression in PC3 cells was also increased in response to stress induced by serum withdrawal, suggesting that miR-182 upregulation can occur due to nutritional stress. Bcl2 and p21 were identified to be potential target genes of miR-182 in PC3 cells. Bcl2 was downregulated and p21 was upregulated in PC3 cells exposed to ATO. These data suggest that miR-182 may be a stress-responsive miRNA that mediates ATO action in prostate cancer cells. Gene and miRNA expression in two prostate cancer cell lines treated with Atorvastatin vs. untreated control.
2013-09-30 | E-GEOD-46374 | biostudies-arrayexpress