PAX5 promotes progression of neuroendocrine prostate cancer
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA533095 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8908970_1.fastq.gz | Fastqsanger.gz | |||
| SRR8908970_2.fastq.gz | Fastqsanger.gz | |||
| SRR8908971_1.fastq.gz | Fastqsanger.gz | |||
| SRR8908971_2.fastq.gz | Fastqsanger.gz | |||
| SRR8908966_1.fastq.gz | Fastqsanger.gz |
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Project description:Neuroendocrine-like differentiation of castration-resistant prostate cancer is highly aggressive and independent of the androgen receptor signaling for its progression. During such lineage differentiation, adenocarcinoma adopts basal and neuronal characteristics that alter its clinical progression, limiting its therapeutic opportunities. Inadequate understanding of the molecular mechanism for such transformation also restricts its targeted therapies. Using ATAC-Seq, acetylated-histone ChIP-seq, and RNA-seq, we have characterized the early transformation process and identified chromatin occupancy and gene expression differences between adenocarcinoma and neuroendocrine-like cancer cells. By comparing differentially active promoter signatures during lineage-specific transcriptional events, our results indicate that the transcription factor Pax5 plays a major role in the trans-differentiation processes. Using LuCaP PDX tissues and metastatic prostate cancer TMA, in conjunction with patient RNA-expression databases, we validated that Pax5 is selectively expressed only in neuroendocrine like cancer but not in adenocarcinoma. Further analysis reveals that Pax5 expression is involved in neuronal gene expression and critical for imparting therapy resistance. Further, our results indicate that increased hydroxymethylation at the Pax5 promoter leads to recruitment of the homeobox transcription factor Pbx1 for Pax5 transcription. This is in line with our findings that lineage-specific expression of Pbx1/Pax5 is associated with the development of neuroendocrine-like differentiation. Our study suggests, upon continuous exposure to anti-androgen therapeutic stress, chromatin modifications are associated with Pax5-mediated gene expression to adopt neuroendocrine-like characteristics of advanced prostate cancer.
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Project description:Neuroendocrine-like differentiation of castration-resistant prostate cancer is highly aggressive and independent of the androgen receptor signaling for its progression. During such lineage differentiation, adenocarcinoma adopts basal and neuronal characteristics that alter its clinical progression, limiting its therapeutic opportunities. Inadequate understanding of the molecular mechanism for such transformation also restricts its targeted therapies. Using ATAC-Seq, acetylated-histone ChIP-seq, and RNA-seq, we have characterized the early transformation process and identified chromatin occupancy and gene expression differences between adenocarcinoma and neuroendocrine-like cancer cells. By comparing differentially active promoter signatures during lineage-specific transcriptional events, our results indicate that the transcription factor Pax5 plays a major role in the trans-differentiation processes. Using LuCaP PDX tissues and metastatic prostate cancer TMA, in conjunction with patient RNA-expression databases, we validated that Pax5 is selectively expressed only in neuroendocrine like cancer but not in adenocarcinoma. Further analysis reveals that Pax5 expression is involved in neuronal gene expression and critical for imparting therapy resistance. Further, our results indicate that increased hydroxymethylation at the Pax5 promoter leads to recruitment of the homeobox transcription factor Pbx1 for Pax5 transcription. This is in line with our findings that lineage-specific expression of Pbx1/Pax5 is associated with the development of neuroendocrine-like differentiation. Our study suggests, upon continuous exposure to anti-androgen therapeutic stress, chromatin modifications are associated with Pax5-mediated gene expression to adopt neuroendocrine-like characteristics of advanced prostate cancer.
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Project description:Neuroendocrine-like differentiation of castration-resistant prostate cancer is highly aggressive and independent of the androgen receptor signaling for its progression. During such lineage differentiation, adenocarcinoma adopts basal and neuronal characteristics that alter its clinical progression, limiting its therapeutic opportunities. Inadequate understanding of the molecular mechanism for such transformation also restricts its targeted therapies. Using ATAC-Seq, acetylated-histone ChIP-seq, and RNA-seq, we have characterized the early transformation process and identified chromatin occupancy and gene expression differences between adenocarcinoma and neuroendocrine-like cancer cells. By comparing differentially active promoter signatures during lineage-specific transcriptional events, our results indicate that the transcription factor Pax5 plays a major role in the trans-differentiation processes. Using LuCaP PDX tissues and metastatic prostate cancer TMA, in conjunction with patient RNA-expression databases, we validated that Pax5 is selectively expressed only in neuroendocrine like cancer but not in adenocarcinoma. Further analysis reveals that Pax5 expression is involved in neuronal gene expression and critical for imparting therapy resistance. Further, our results indicate that increased hydroxymethylation at the Pax5 promoter leads to recruitment of the homeobox transcription factor Pbx1 for Pax5 transcription. This is in line with our findings that lineage-specific expression of Pbx1/Pax5 is associated with the development of neuroendocrine-like differentiation. Our study suggests, upon continuous exposure to anti-androgen therapeutic stress, chromatin modifications are associated with Pax5-mediated gene expression to adopt neuroendocrine-like characteristics of advanced prostate cancer.
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Project description:PAX5 controls lineage transitions between neuroendocrine and non-neuroendocrine states during carcinoma progression
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Project description:Neuroendocrine prostate cancer (NEPC) is proliferative, invasive, and untreatable. Its molecular pathogenesis remains poorly understood but appears to require TP53 and RB1 aberration. In this study we modeled the development of NEPC from conventional prostatic adenocarcinoma using a unique patient-derived xenograft and identified up-regulation of the placental gene PEG10. We found that the androgen receptor and the E2F/RB pathway dynamically regulate distinct post-transcriptional and post-translational isoforms of PEG10 at different stages of NEPC development. In vitro, PEG10 promoted cell cycle progression from G0/G1 in the context of TP53 loss, and regulated Snail expression via TGF-β signaling to promote invasion. Finally we show in vivo proof of principal using antisense oligonucleotide that PEG10 is a novel therapeutic target for NEPC. Six patient-derived xenograft tumors from the LTL331 xenograft lineage (PMID: 24356420; http://www.livingtumorcentre.com/) after differing lengths of time post-host castration. No replicates.
2015-01-05 | E-GEOD-59985 | biostudies-arrayexpress
Project description:Neuroendocrine prostate cancer (NEPC) is proliferative, invasive, and untreatable. Its molecular pathogenesis remains poorly understood but appears to require TP53 and RB1 aberration. In this study we modeled the development of NEPC from conventional prostatic adenocarcinoma using a unique patient-derived xenograft and identified up-regulation of the placental gene PEG10. We found that the androgen receptor and the E2F/RB pathway dynamically regulate distinct post-transcriptional and post-translational isoforms of PEG10 at different stages of NEPC development. In vitro, PEG10 promoted cell cycle progression from G0/G1 in the context of TP53 loss, and regulated Snail expression via TGF-? signaling to promote invasion. Finally we show in vivo proof of principal using antisense oligonucleotide that PEG10 is a novel therapeutic target for NEPC. 14 patient-derived xenograft tumors from the LTL331 xenograft lineage (PMID: 24356420; http://www.livingtumorcentre.com/) after differing lengths of time post-host castration. Three replicates present for days 1-3 post-host castration.
2015-01-05 | E-GEOD-59984 | biostudies-arrayexpress