ATGL deletion in castration-resistant prostate cancer cell line
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1016447 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26059008_1.fastq.gz | Fastqsanger.gz | |||
| SRR26059008_2.fastq.gz | Fastqsanger.gz | |||
| SRR26059009_1.fastq.gz | Fastqsanger.gz | |||
| SRR26059009_2.fastq.gz | Fastqsanger.gz | |||
| SRR26059010_1.fastq.gz | Fastqsanger.gz |
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Project description:Lipid metabolism plays a central role in prostate cancer. To date, the major focus on prostate cancer lipid metabolism has centered on the roles of de novo lipogenesis and lipid uptake with little consideration for how cancer cells access these lipids once they are created or taken up and stored. Analysis of patient-derived phosphoproteomics data identified adipose triglyceride lipase (ATGL), a rate-limiting enzyme in the breakdown of triglycerides and previously suspected tumor suppressor, as a target of calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2)-AMP-dependent protein kinase (AMPK) signaling that, conversely, promotes castration-resistant prostate cancer (CRPC) progression. Phosphorylation of ATGL by CAMKK2-AMPK signaling increased ATGL’s lipase activity, cancer cell proliferation, migration, and invasion. Shotgun lipidomics and imaging mass spectrometry demonstrated ATGL’s profound regulation of prostate cancer lipid metabolism in vitro and in vivo, remodeling membrane composition. Targeting ATGL using molecular, genetic, and/or pharmacological approaches impaired the growth of human and murine prostate cancer cells in culture and xenograft mouse models of CRPC as well as organoid models. The efficacy of ATGL inhibition occurs in a glucose concentration-dependent manner. Accordingly, pharmacological inhibition or depletion of ATGL induced metabolic plasticity with a shift towards glycolysis, which could be exploited therapeutically by co-targeting both metabolic pathways. Together, these data nominate ATGL and intracellular lipolysis as a potential therapeutic target for the treatment of CRPC and provide insights for future combination therapies.
2023-11-22 | GSE243159 | GEO
Project description:Purpose: Resistance to androgen deprivation therapies is a major driver of mortality in advanced prostate cancer. Therefore, there is a need to develop new pre-clinical models that allow the investigation of resistance mechanisms and the assessment of drugs for the treatment of castration resistant prostate cancer. Methods: We generated two novel cell line models (LAPC4-CR and VCaP-CR) which were derived by passaging LAPC4 and VCaP cells in vivo and in vitro under castrate conditions. We performed detailed transcriptomic (RNA-seq) to delineate expression differences between castration-sensitive and castration-resistant cell lines. LAPC4-CR and VCaP-CR cell lines maintained AR expression, but exhibited distinct expression changes on the mRNA and protein level. Integrated analyses including data from LNCaP and the previously described castration resistant LNCaP-abl cells revealed an expression signature of castration resistance. Results: Integrated analyses including data from LNCaP and the previously described castration resistant LNCaP-abl cells revealed an expression signature of castration resistance.
2021-06-27 | GSE178963 | GEO
Project description:TMT-MS of whole cell lysate collected from 22Rv1 castration-resistant prostate cancer cells treated with 5 µM JG-98 for 4 hours.
2023-04-25 | PXD038684 | JPOST Repository
Project description:The integration of diverse ‘omic’ datasets will increase our understanding of the key signaling pathways that drive disease. Here, we used clinical tissue cohorts corresponding to lethal metastatic castration resistant prostate cancer (CRPC) obtained at rapid autopsy to integrate mutational, transcriptomic, and phosphoproteomic datasets for pathway analysis. Using Tied Diffusion through Interacting Events (TieDIE), we integrated differentially expressed transcriptional master regulators, functionally mutated genes, and differentially ‘activated’ kinases in CRPC tissues to synthesize a robust signaling network consisting of pathways with known and novel gene interactions. For 6 individual CRPC patients for which we had transcriptomic and phosphoproteomic data we observed distinct pathway activation states for each patient profile. In one patient, the activated pathways were strikingly similar to a prostate cancer cell line, 22Rv1, providing us with a good pre-clinical model to test targeted, combination therapies. In all, synthesis of multiple ‘omic’ datasets revealed a plethora of pathway information suitable for targeted therapies in lethal prostate cancer.
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Project description:Peripheral blood from 62 men with castration resistant prostate cancer was collected between 8/2006 and 6/2008. A panel of 168 inflammation-related and prostate cancer related genes was assessed with quantitative PCR to assess biomarkers predictive of survival. qPCR profiling of whole blood from patients with castration-resistant prostate cancer.
2013-04-02 | E-GEOD-45705 | biostudies-arrayexpress
Project description:Prostate cancer is one of the major cancers that seriously affect men's health. It has high morbidity and high mortality, but there is still no ideal molecular markers for the diagnosis and prognosis of prostate cancer. Castration-resistant prostate cancer is associated with wide variations in survival. To determine whether differentially expressed circRNAs in plasma exosomes can be used as a novel biomarker for castration-resistant prostate cancer prognosis, we performed high-throughput circRNA sequencing on 15 pairs of plasma exosomes from 30 metastatic castration-resistant prostate cancer patients, with or without early progression, to screen differentially expressed circRNAs.
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Project description:Relatively little is known about how changes in gene copy number (CN) and gene CpG methylation interact to affect specific pathways in metastatic castration-resistant prostate cancer (CRPC). Oligonucleotide array comparative genomic hybridization (aCGH) was performed on DNA isolated from 15 metastatic CRPC samples. Commonly aberrant genes were evaluated in a confirmatory fashion using PCR, aCGH data from primary tumors, and existing CRPC expression data. Array-based comprehensive CpG methylation was assessed on the same sample set. A total of 495 genes (79 gained, 416 deleted) were CN aberrant in ?66% of the samples by aCGH, and 77 (9 amplified, 68 deleted) had statistically concordant expression including gain of AR and loss of PTEN and RB1. Significant CN differences were seen between the genomes of patients with AR-amplified and AR-unamplified tumors, including common loss of AR repressors in AR-unamplified tumors. The majority of CRPC samples were hypermethylated compared to benign prostate tissue. Simultaneous methylation and heterozygous gene deletion occurred in the tumor suppressor RB1 and in HSD17B2, responsible for testosterone metabolism. Establishment of a comprehensive methylation signature and coupling of epigenomic and structural analyses sheds light on the alterations that allow CRPC to circumvent hormonal therapy and may provide new drug targets for what is currently an incurable disease state. 15 tumor samples taken from 14 men with metastatic castration resistant prostate cancer were analyzed, including two samples from the same patient. No control samples were used for this experiment.
2011-12-06 | E-GEOD-34174 | biostudies-arrayexpress
Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. Androgen-deprivation therapy is the first-line treatment strategy for advanced prostate cancer. However, many tumors develop to castration-resistant prostate cancer (CRPC) and relapse. Thus, analyzing key factors for development of CRPC is important. We found PSF functions as RNA binding protein and transcription factor to promote castration-resistant tumor growth. High expression of PSF in metastatic prostate cancer tissue indicates the clinical relevance. In order to investigate the PSF function in CRPC cells, we performed gene expression in CRPC model cells derived from AR-positive prostate cancer cell lines after siPSF treatment.
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Project description:The transcription factor GATA2 regulates chemotherapy resistance in prostate cancer. We report a novel GATA2 transcriptional program that has implications for chemotherapy resistance disease and aggressiveness in castration resistant prostate cancer.
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Project description:To identify changes at multiple omic levels between hormone naive and castration resistant prostate cancer. Using orthograft murine tumour models of human cell lines injected into the prostate of CD-1 Nude mice grown under castration resistant (castrate) or hormone naive (non-castrate) conditions.
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