Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Novel Race-specific Genetic and Epigenetic Determinants of ADT-Resistance in African American Prostate Cancer

ABSTRACT: Purpose: The goals of this study is to compare NGS-derived Androgen Deprivation Therapy (ADT) resistant miRNome profiling to Androgen Deprivation Therapy (ADT) sensitive miRNome profile in African American prostate cancer cells and validate by reverse transcription polymerase chain reaction (qRT–PCR) methods. Method: Mirco-RNA were isolated from different CaP cells who were sensitive and resistant to Androgen Deprivation Therapy (ADT). Total micro-RNA were subjected to miRNA-Seq. Results: We performed whole miRNA-Seq analysis through paired-end deep sequencing to systematically investigate the molecular features of different CaP cell models- RC-77-N, RC-77T/E, RCC7T/E-ADT, RCC7T/E-CD133-plus, E006AA-hT and E006AA-hT-ADT. Conclusions: Our study represents the first detailed analysis of African American ADT resistant miRNome, with biologic replicates, generated by miRNA-seq technology.

ORGANISM(S): Homo sapiens

PROVIDER: GSE116636 | GEO | 2019/07/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Race-specific transcriptome and Long non-coding RNA of ADT-resistant African-American prostate cancer cell models.

Project description:Purpose: The goals of this study are to compare NGS-derived Androgen Deprivation Therapy (ADT) resistant transcriptome to profiling (RNA-seq) to Androgen Deprivation Therapy (ADT) sensitive transcriptome in African American prostate cancer cells and validate by reverse transcription polymerase chain reaction (qRT–PCR) methods. Method: Total RNA was extracted from different CaP cell who were ADT sensitive and ADT resistance. Total RNA was subjected to whole transcriptome sequencing analysis. Sequence reads Results: We performed whole transcriptome RNA-Seq analysis through paired-end deep sequencing to systematically investigate the molecular features of different CaP cell models- RCC7/N, RCC7T/E, RCC7T/E-ADT, RCC7T/E-CD133, E006AA-hT and E006AA-hT-ADT We obtained an average of 23.85 million reads per sample, ranging from 22.86 to 24.93 million reads, with an average mapping rate of 98.29% to the reference human genome (UCSC version hg20). Next we performed Kal’s Z-test and generated Fold-Change (FC) values, p values and False Discovery Rate (FDR) values for measuring comparative gene expression profile. By applying stringent statistical threshold of greater than or equal to 2 FC, p value < 0.05 and FDR value < 1, we identified genes that were significantly differentially expressed in three different comparative groups. Conclusions: "Our study represents the first detailed analysis of African American ADT resistant transcriptomes, with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. Our results show that NGS offers a comprehensive and more accurate quantitative and qualitative evaluation of mRNA content within a cell or tissue. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions. "

2019-07-09 | GSE115307 | GEO

Next generation sequencing of advanced non-castrate prostate cancer treated with docetaxel chemotherapy

Project description:Early chemotherapy for advanced/metastatic non-castration resistant prostate cancer (PCa) may improve overall patient survival. We studied the safety, tolerability and early efficacy of up-front docetaxel chemotherapy and androgen deprivation therapy (ADT) versus ADT alone for patients with newly-diagnosed advanced/metastatic PCa. As proof of concept, we undertook in vivo gene expression profiling by next generation RNA sequencing (RNA-Seq). Tumour biposies from 6 patients were taken before and after treatment with combined ADT and docetaxcel for 6 weeks

2014-09-18 | E-GEOD-51005 | biostudies-arrayexpress

NCOR2 controls androgen deprivation therapy failure in advanced prostate cancer through re-wiring of the onco-epigenome [RNA-seq]

Project description:NCOR2 is frequently and significantly mutated in late stage androgen deprivation therapy resistant prostate cancer (ADT-RPCa). NCOR2 has been characterized as a transcriptional corepressor and has mechanistic links to DNA methylation, but its global functions and overall contributions to PCa progression remain enigmatic. We mapped the dihydrotestosterone (DHT) dependent and independent effects of NCOR2 on the transcriptome, cistrome and DNA methylome in androgen sensitive (AS) and ADT-RPCa cells using the isogenic LNCaP and LNCaP-C4-2 (C4-2) cell models and the CWR22 xenograft model of ADT-RPCa.

2021-11-17 | GSE180373 | GEO

NCOR2 controls androgen deprivation therapy failure in advanced prostate cancer through re-wiring of the onco-epigenome [ChIP-seq]

2021-11-17 | GSE180372 | GEO

NCOR2 controls androgen deprivation therapy failure in advanced prostate cancer through re-wiring of the onco-epigenome [CWR22 xenograft]

2021-11-17 | GSE179133 | GEO

NCOR2 controls androgen deprivation therapy failure in advanced prostate cancer through re-wiring of the onco-epigenome [CWR22_EPIC]

2021-11-17 | GSE178819 | GEO

NCOR2 controls androgen deprivation therapy failure in advanced prostate cancer through re-wiring of the onco-epigenome [CellLine_EPIC]

2021-11-17 | GSE178818 | GEO

Next generation sequencing of advanced non-castrate prostate cancer treated with docetaxel chemotherapy

2014-09-18 | GSE51005 | GEO

Dynamic interplay between sortilin and syndecan-1 has a role in the metabolic switch during prostate cancer progression

Project description:Prostate cancer development and progression relies on the programming of glucose and lipid metabolism, and this involves alterations in androgen receptor expression and signalling. Androgen deprivation therapy (ADT) provides short-term efficacy for patient treatment, but inevitably promotes a castration-resistant phenotype with poor prognosis. Defining the molecular mechanism that underpins this metabolic programming will have direct significance for prostate cancer patients who have poor expected outcomes and/or receive ADT. Here we show that there is a dynamic balance between sortilin and syndecan-1 that reports on different metabolic phenotypes. Sortilin, enhances glucose metabolism by regulating GLUT1 and GLUT4, while binding progranulin and lipoprotein lipase (LPL) to limit lipid metabolism. In contrast, syndecan-1 interacts with LPL and β3 integrin, to promote lipid metabolism and this process is upregulated in androgen-insensitive cells. We report a hitherto unappreciated molecular mechanism for prostate cancer, which has significance for disease progression and how ADT may promote castration-resistant prostate cancer.

2023-08-21 | GSE220618 | GEO

Modeling androgen deprivation therapy-induced prostate cancer dormancy and its clinical implications

Project description:Purpose: Treatment-induced tumor dormancy is a state in cancer progression where residual disease is present but remains asymptomatic. Dormant cancer cells are treatment-resistant and responsible for cancer recurrence and metastasis. Prostate cancer (PCa) treated with androgen-deprivation therapy (ADT) often enters a dormant state. ADT-induced PCa dormancy remains poorly understood due to the challenge in acquiring clinical dormant PCa cells and the lack of representative models. We, therefore, aimed to develop clinically relevant models that can be used for studying ADT-induced PCa dormancy. Experimental design: Dormant PCa models were established by castrating mice bearing PCa patient-derived xenografts (PDXs) of hormonal naïve or sensitive PCa. Dormancy status and tumor relapse were monitored and evaluated. Paired pre- and post-castration (dormant) PDX tissues were subjected to morphological and transcriptome profiling analyses. Results: We established eleven ADT-induced dormant PCa models that closely mimicked the clinical courses of ADT-treated PCa. We identified two ADT-induced dormancy subtypes that differed in morphology, gene expression, and relapse rates. We discovered transcriptomic differences in pre-castration PDXs that predisposed the dormancy response to ADT. We further developed a dormancy subtype-based, predisposed gene signature that was significantly associated with ADT response in hormonal naïve PCa and clinical outcome in castration-resistant PCa treated with ADT or androgen-receptor pathway inhibitors.

2022-01-11 | GSE193500 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data