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The EP4 antagonist vorbipiprant and an anti-PD-1 in MSS mCRC

ABSTRACT: The EP4 antagonist vorbipiprant and an anti-PD-1 in MSS mCRC

PROVIDER: PRJNA1183748 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31284626_1.fastq.gz	Fastqsanger.gz
	SRR31284626_2.fastq.gz	Fastqsanger.gz
	SRR31284627_1.fastq.gz	Fastqsanger.gz
	SRR31284627_2.fastq.gz	Fastqsanger.gz
	SRR31284628_1.fastq.gz	Fastqsanger.gz

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The EP4 antagonist vorbipiprant and an anti-PD-1 in MSS mCRC

Project description:The aim of the study was to determine whether vorbipiprant, a prostaglandin EP4 receptor antagonist, can convert immune-resistant mCRC into a tumor responsive to anti-PD-1 inhibition

2024-11-12 | GSE281374 | GEO

Gene expression profiles in CT26 syngeneic tumor tissues after EP4 antagonist TP-16(BY001), anti-PD-1 antibody or combination treatment

Project description:To explore the mechanisms resposible for the synergistic effect between EP4 antagonist BY001 and anti-PD-1 antibody, we conducted a microarray analysis on gene expression profiles in CT26 syngenetic tumor tissues. We used Agilent SurePrint G3 Mouse GE V2.0 Array to detail gene expression after indicated treatments and identified the molecular mechanism during this process to facilitate further studies.

2020-10-19 | GSE132004 | GEO

Gene expression profiles in CT26 syngeneic tumor tissues after EP4 antagonist TP-16(BY001), anti-PD-1 antibody or combination treatment

Project description:Gene expression profiles in CT26 syngeneic tumor tissues after EP4 antagonist TP-16(BY001), anti-PD-1 antibody or combination treatment

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Identification of EP4 as a Potential Target for the Treatment of Castration-Resistant Prostate Cancer Using a Novel Xenograft Model

Project description:More effective therapeutic approaches for castration-resistant prostate cancer (CRPC) are urgently needed, thus reinforcing the need to understand how prostate tumors progress to castration resistance. We have established a novel mouse xenograft model of prostate cancer, KUCaP-2, which expresses the wild-type androgen receptor (AR) and which produces the prostate-specific antigen (PSA). In this model, tumors regress soon after castration, but then reproducibly restore their ability to proliferate after 1 to 2 months without AR mutation, mimicking the clinical behavior of CRPC. In the present study, we used this model to identify novel therapeutic targets for CRPC. Evaluating tumor tissues at various stages by gene expression profiling, we discovered that the prostaglandin E receptor EP4 subtype (EP4) was significantly upregulated during progression to castration resistance. Immunohistochemical results of human prostate cancer tissues confirmed that EP4 expression was higher in CRPC compared with hormone-naÃ¯ve prostate cancer. Ectopic overexpression of EP4 in LNCaP cells (LNCaP-EP4 cells) drove proliferation and PSA production in the absence of androgen supplementation in vitro and in vivo. Androgen-independent proliferation of LNCaP-EP4 cells was suppressed when AR expression was attenuated by RNA interference. Treatment of LNCaP-EP4 cells with a specific EP4 antagonist, ONO-AE3-208, decreased intracellular cyclic AMP levels, suppressed PSA production in vitro, and inhibited castration-resistant growth of LNCaP-EP4 or KUCaP-2 tumors in vivo. Our findings reveal that EP4 overexpression, via AR activation, supports an important mechanism for castration-resistant progression of prostate cancer. Furthermore, they prompt further evaluation of EP4 antagonists as a novel therapeutic modality to treat CRPC. 4 samples in each group: androgen-dependent growth (AD), castration-induced regression nadir (ND), and castration-resistant regrowth (CR) stages

2010-06-08 | E-GEOD-21887 | biostudies-arrayexpress

Identification of EP4 as a Potential Target for the Treatment of Castration-Resistant Prostate Cancer Using a Novel Xenograft Model

Project description:More effective therapeutic approaches for castration-resistant prostate cancer (CRPC) are urgently needed, thus reinforcing the need to understand how prostate tumors progress to castration resistance. We have established a novel mouse xenograft model of prostate cancer, KUCaP-2, which expresses the wild-type androgen receptor (AR) and which produces the prostate-specific antigen (PSA). In this model, tumors regress soon after castration, but then reproducibly restore their ability to proliferate after 1 to 2 months without AR mutation, mimicking the clinical behavior of CRPC. In the present study, we used this model to identify novel therapeutic targets for CRPC. Evaluating tumor tissues at various stages by gene expression profiling, we discovered that the prostaglandin E receptor EP4 subtype (EP4) was significantly upregulated during progression to castration resistance. Immunohistochemical results of human prostate cancer tissues confirmed that EP4 expression was higher in CRPC compared with hormone-naïve prostate cancer. Ectopic overexpression of EP4 in LNCaP cells (LNCaP-EP4 cells) drove proliferation and PSA production in the absence of androgen supplementation in vitro and in vivo. Androgen-independent proliferation of LNCaP-EP4 cells was suppressed when AR expression was attenuated by RNA interference. Treatment of LNCaP-EP4 cells with a specific EP4 antagonist, ONO-AE3-208, decreased intracellular cyclic AMP levels, suppressed PSA production in vitro, and inhibited castration-resistant growth of LNCaP-EP4 or KUCaP-2 tumors in vivo. Our findings reveal that EP4 overexpression, via AR activation, supports an important mechanism for castration-resistant progression of prostate cancer. Furthermore, they prompt further evaluation of EP4 antagonists as a novel therapeutic modality to treat CRPC.

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Epithelial EP4 plays an essential role in maintaining homeostasis in colon

Project description:The EP4 receptor is known to mediate the protective effect of prostaglandin (PG) E2 in the gastrointestinal tract; however, the exact role of epithelial EP4 in intestinal pathophysiology remains unknown. We investigated the role of epithelial EP4 in maintaining colonic homeostasis by characterizing the intestinal epithelial cell-specific EP4 knockout (EP4 cKO) mice. We found a significant enrichment of genes involved in apoptosis-related pathways in the EP4 cKO colons. Moreover, inflammation-associated pathways were highly enriched and revealed more than half of the top 20 pathways related to immune response.

2019-10-29 | GSE135859 | GEO

High- and Low-dose Radiotherapy Combined With PD-1 Inhibitors for MSS CRLM

Project description:This pilot phase I trial aims to investigate the efficacy and safety of high- and low-dose radiotherapy combined with programmed cell death-1 (PD-1) inhibitors in microsatellite stable (MSS) metastatic colorectal cancer (mCRC) that have failed second-line immunotherapy or above.

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Rhodococcus EP4 Aromatic Transcriptomics

Project description:Rhodococcus EP4 Aromatic Transcriptomics

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