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NQO1 regulates inflammatory signaling

ABSTRACT: NQO1 silencing by a specific shRNA against NQO1 increased migration and hormone-independent survival in hormone-dependent human prostate cancer cells LNCaP. Genome wide array revealed that NQO1 blockade significantly upregulated pro-inflammatory mediators (e.g., IL-32, CCL2, IL-8, IL-17C, IL-10RA, CXCR2, CXCR7, NOS3) associated with prostate tumorigenesis. Two-condition experiment, control vs. NQO1 knockdown LNCaP cells. Biological replicates: 3 control replicates, 3 NQO1 knockdown replicates.

ORGANISM(S): Homo sapiens

SUBMITTER: Rita Ghosh

PROVIDER: E-GEOD-58336 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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NQO1 suppresses NF-κB-p300 interaction to regulate inflammatory mediators associated with prostate tumorigenesis.

Thapa Dinesh D Meng Peng P Bedolla Roble G RG Reddick Robert L RL Kumar Addanki P AP Ghosh Rita R

Cancer research 20140814 19

NADPH reductase<h4>Nad(p)h</h4>quinone oxidoreductase 1 (NQO1) is needed to maintain a cellular pool of antioxidants, and this enzyme may contribute to tumorigenesis on the basis of studies in NQO1-deficient mice. In this work, we sought deeper insights into how NQO1 contributes to prostate carcinogenesis, a setting in which oxidative stress and inflammation are established contributors to disease development and progression. In the TRAMP mouse model of prostate cancer, NQO1 was highly expressed ...[more]

PMID: 25125658

Similar Datasets

NQO1 regulates inflammatory signaling

Project description:NQO1 silencing by a specific shRNA against NQO1 increased migration and hormone-independent survival in hormone-dependent human prostate cancer cells LNCaP. Genome wide array revealed that NQO1 blockade significantly upregulated pro-inflammatory mediators (e.g., IL-32, CCL2, IL-8, IL-17C, IL-10RA, CXCR2, CXCR7, NOS3) associated with prostate tumorigenesis.

2014-08-26 | GSE58336 | GEO

Quorum sensing in CD4+ T cells homeostasis : IL-2 coordinates the interplay between IL-2p and regulatory T cells.

Project description:Many species of bacteria use quorum sensing to sense the amounts of secreted metabolites and adapt their growth according to their population density. We asked whether similar mechanisms would operate in lymphocyte homeostasis. We investigated the regulation of the size of Interleukin-2-producing CD4+ T-cell (IL-2p) pool using different IL-2-reporter mice. We found that in the absence of either IL-2 or regulatory CD4+ T-cells (Treg) the number of IL-2p-cells increases. Administration of IL-2 decreases the number of cells of the IL-2p-cell subset and pertinently, abrogates their ability to produce IL-2 upon in vivo cognate stimulation, while increasing Treg-cell numbers. We propose that control of the IL-2p-cell numbers occurs via a quorum-sensing-like feedback loop where the produced IL-2 is sensed by both the activated CD4+ T-cell pool and by Treg-cells, which reciprocally regulate cells of the IL-2p-cell subset. In conclusion, IL-2 acts as a self-regulatory circuit integrating the homeostasis of activated and regulatory T cells as CD4+ T-cells restrain their growth by monitoring IL-2 levels thereby preventing uncontrolled responses and autoimmunity. 2 populations of conventional CD4+ T cell are analysed. 5 replicates for each. GFP- is the control one.

2013-11-01 | E-GEOD-50149 | biostudies-arrayexpress

Relation between T CD4+: Regulatory cells and IL-2 producing cells

Project description:We previously proposed that lymphocyte homeostasis is achieved by a quorum-sensing like mechanism, based on the paracrine sensing of IL-2 by Foxp3(+) regulatory T CD4(+) cells. In turn, these cells will suppress IL-2 producing cells, thereby controlling the total number of T CD4(+) cells. As CD4(+) T regulatory cells are unable to produce IL-2, such control mechanism assumes the complete segregation of both lymphocyte subsets, that is to say they constitute distinct compartments. In the present study, we re-evaluate the above-described quorum-sensing mechanism by considering the non-exclusive possibility that a fraction of IL-2-producing cells might acquire regulatory function, implying the existence of a role for an autocrine sensing of IL-2 in the homeostasis of the regulatory compartment. According to the mouse models used in these experiments, RFP is used as a reporter for the Foxp3 expression. The transcription factor Foxp3 is the main hallmark of T CD4(+) regulatory cells. Therefore RFP(+) cells are associated to T CD4(+) regulatory cells. According to the mouse model, and our last publication (PMID: 24249704), the GFP is a reporter for cells that having activated the IL-2 locus within the last 2-3 weeks. This subset of cells is called IL-2p cells. 4 populations of conventional CD4+ T cell are analysed. 5 replicats for each.

2015-02-01 | E-GEOD-54686 | biostudies-arrayexpress

A regulatory CD9+ B cell subset controls HDM-induced allergic airway inflammation

Project description:Background: A specific subset of regulatory IL-10 producing B cells has been extensively studied in autoimmune and inflammatory pathologies. These cells are able to constrain exacerbated inflammation by inhibiting T cell mediated responses and maturation of antigen presenting cells. In allergic diseases, observations that increase of regulatory B cells is necessary for allergen tolerance suggest that development of allergic asthma would be associated with a defect in the regulatory B cells compartment. Objective: We sought to (i) characterize regulatory IL-10+ regulatory B cell subset in Balb/c mice by microarray and flow cytometry and (ii) investigate their regulatory capacity in vivo in a house dust mite model of allergic asthma. Results: We identified an IL-10 producing B cells subset able to control T cell proliferation in vitro in both control and asthmatic mice. This subset is decreased in allergic mice. IL-10+ Breg cells express high levels of CD9 and upregulate CD70 and CD73 after activation. Expression of CD9 allows identifying more than 50% of Bregs. Interestingly CD9+ B cells inhibit TH2-TH17 allergic airway inflammation in vivo after adoptive transfer in an IL-10 dependent manner. Conclusions: Herein, we demonstrate that induction of allergic asthma dampens the generation of Bregs contributing to exacerbated airway inflammation. We identified a distinct CD9+ Breg-cell population decreased in lung of HDM mice and able to control asthma and allergic airway inflammation by producing IL-10 after adoptive transfer. This study points B cells as an interesting therapeutic target in allergic asthma. IL-10+ B cells (n=3) and 3 IL-10- B cells (n=3) in control mice + IL-10+ B cells (n=3) and 3 IL-10- B cells (n=3) from asthmatic allergic (HDM) mice

2015-03-01 | E-GEOD-57772 | biostudies-arrayexpress

Ligand-independent CXCR7 Activation of MAPK Signaling leads to Prostate Cancer Enzalutamide Resistance

Project description:The standard of care for patients with advanced form of prostate cancer, castration-resistant, now includes enzalutamide, a second generation antiandrogen. However, most of the treated patients will develop resistance to enzalutamide based therapy in around a year, succumbing to lethal disease. Investigating the transcriptome of enzalutamide-resistant prostate cancer cell lines, we identified CXCR7 as one of the most upregulated genes suggesting its role in advanced prostate cancer. CXCR7, known as an atypical G-coupled receptor, is engaged in many physiological and pathological processes. Here we show that in prostate cancer CXCR7 is tightly regulated by androgen receptor (AR), which directly binds to CXCR7 gene promoter and enhancer and represses its transcription. In turn, CXCR7 in prostate cancer reduces enzalutamide toxicity and promotes cell survival and invasiveness. We identified that CXCR7 forms an integral complex with ARRB2 and activates ERK1/2, eliciting pro-survival MAPK pathway. Enzalutamide treatment combined with MAPKK specific inhibitor, trametinib, reversed enzalutamide resistance in prostate cancer in vitro and in vivo. Taken together our findings highlight the critical role of CXCR7 in enzalutamide-resistant prostate cancer and open an avenue for developing novel anti-CXCR7 therapies to improve survival in patients with advanced prostate cancer.

2019-04-06 | GSE104935 | GEO

Expression data of LNCaP and MDA PCa 2b cells in absence or presence of IL6

Project description:Prostate cancer (PCa) development and progression are associated with chronic inflammation. The cytokine interleukin (IL)-6 can influence progression, differentiation, survival, and angiogenesis of PCa. To identify novel pathways that are triggered by IL-6, we performed a gene expression profiling of two PCa cell lines, LNCaP and MDA PCa 2b, under treatment with 5 ng/ml IL-6. Interferon regulatory factor (IRF)9 was identified as one of the most prevalent IL-6 regulated genes in both cell lines. IRF9 is a mediator of type I interferon signaling and acts together with signal transduction and activator of transcription (STAT)1 and 2 to activate transcription of interferon responsive genes. The IL-6 regulation of IRF9 was confirmed at mRNA and protein levels by quantitative real-time PCR and Western blot, respectively, in both cell lines and could be blocked by the anti-IL-6 antibody Siltuximab. Three PCa cell lines with an autocrine IL-6 loop, PC3, DU145, and LNCaP-IL-6+, showed a high expression of IRF9. A tissue microarray with 36 malignant and adjacent 36 benign areas from prostate cancer specimens showed that IRF9 protein expression is moderately elevated in malignant areas and positively correlates with the tissue expression of IL-6. Downregulation and overexpression of IRF9 provided evidence for an interferon-independent role of IRF9 on cellular proliferation of different PCa cell lines. Furthermore, expression of IRF9 was essential to mediate the antiproliferative effects of IFN-M-NM-12. We concluded that IL-6 is an inducer of IRF9 expression in prostate cancer and a sensitizer for the antiproliferative effects of IFNM-NM-12. LNCaP and MDA PCa 2b cells were seeded in 12 wells each. The cells were starved for 24 h and half were treated with 5 ng/ml IL-6 for 18 h. Two biological replicates were performed, each in three replicates, resulting in 12 samples per cell line.

2013-08-02 | E-GEOD-47973 | biostudies-arrayexpress

Hedgehog/GLI signalling and hormone independence in prostate cancer (PCa) cell lines

Project description:High levels of GLI (GLI1 and GLI2) mRNA and GLI luciferase reporter activity were detected in the androgen independent prostate cancer cell lines DU145 and PC-3 compared to the androgen-dependent LNCaP prostate cancer cell line. Subsequently, we observed that ectopic GLI1 promoted hormone independence in LNCaP cells (LNCaP-GLI1). We compared the gene expression profile of LNCaP-pBP (empty vector), LNCaP-GLI1, DU145, and PC-3 cells globally as well as to identify GLI1-regulated genes that may contribute to hormone independence.

2011-02-13 | GSE27231 | GEO

Prostate cancer cell lines: non-targeting siRNA versus SChLAP1-siRNA treated

Project description:SChLAP1 is a novel long non-coding RNA expressed in prostate cancer. Here we performed transcriptional profiling of the prostate cancer cell lines LNCaP and 22Rv1 comparing non-targeting siRNA treatment versus SChLAP1-siRNA treatment. Goal was to determine the effect of SChLAP1 knockdown on gene expression in prostate cancer. Two-condition experiment: non-targeting siRNA versus SChLAP1 siRNA treated cells. Biological replicates: 1 control replicate, 2 treatment replicates. Technical replicates: 3 replicates per SChLAP1 siRNA. Cell lines: 22Rv1 and LNCaP.

2013-07-20 | E-GEOD-40383 | biostudies-arrayexpress

Hedgehog/GLI signalling and hormone independence in prostate cancer (PCa) cell lines

2011-02-13 | E-GEOD-27231 | biostudies-arrayexpress

Differential Expressions of miRNAs in resting and activated human in vitro-differentiated NK cells

Project description:To investigate miRNA expressions of miRNA upon activation. In vitro-differentiated human NK cells were freshly incubated in the presence of IL15 after 24h deprivation of IL-15. The cells were harvested at the times (0h, resting-Sample 1 and 2; 6h, activated-Sample 3 and 4) and analyzed by microarray.

2011-11-21 | E-GEOD-32411 | biostudies-arrayexpress

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