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Transcriptional analysis of metastatic hormone-naïve prostate cancer primary tumour biopsies reveals a relevant role for SOX11 in prostate cancer cell dissemination [Discovery dataset]

ABSTRACT: Transcriptional analysis of metastatic hormone-naïve prostate cancer primary tumour biopsies reveals a relevant role for SOX11 in prostate cancer cell dissemination [Discovery dataset]

PROVIDER: PRJNA1116142 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29164100_1.fastq.gz	Fastqsanger.gz
	SRR29164100_2.fastq.gz	Fastqsanger.gz
	SRR29164200_1.fastq.gz	Fastqsanger.gz
	SRR29164200_2.fastq.gz	Fastqsanger.gz
	SRR29164101_1.fastq.gz	Fastqsanger.gz

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Transcriptional analysis of metastatic hormone-naïve prostate cancer primary tumour biopsies reveals a relevant role for SOX11 in prostate cancer cell dissemination [Validation dataset]

Project description:Metastatic hormone-naïve prostate cancer (mHNPC) is an infrequent form of this tumour type that is characterized by metastasis at the time of diagnosis and accounts for 50% of prostate cancer-related deaths. Despite the extensive characterization of localized and metastatic castration resistant prostate cancer (mCRPC), the molecular characteristics of mHNPC remain largely unexplored. To characterize the transcriptomic landscape of mHNPC, we generated discovery and validation bulk and single-cell RNA-Seq datasets. We performed integrative computational analysis in combination with experimental studies. Our results provide unprecedented evidence of the distinctive transcriptional profile of mHNPC and identify stroma remodelling as a predominant feature of these tumours. Importantly, we discover a central role for the transcription factor SOX11 in triggering a heterotypic communication that is associated to the acquisition of metastatic properties. Our study will constitute an invaluable resource for a profound understanding of mHNPC that can influence patient management.

2025-04-29 | GSE268309 | GEO

Transcriptional analysis of metastatic hormone-naïve prostate cancer primary tumour biopsies reveals a relevant role for SOX11 in prostate cancer cell dissemination [Discovery dataset]

2025-04-29 | GSE268308 | GEO

Transcriptional analysis of metastatic hormone-naïve prostate cancer primary tumour biopsies reveals a relevant role for SOX11 in prostate cancer cell dissemination [scRNA-Seq]

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Transcriptional analysis of metastatic hormone-naïve prostate cancer primary tumour biopsies reveals a relevant role for SOX11 in prostate cancer cell dissemination [DU145-SOX11overexpression_dataset]

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Transcriptional analysis of metastatic hormone-naïve prostate cancer primary tumour biopsies reveals a relevant role for SOX11 in prostate cancer cell dissemination [scRNA-Seq]

Project description:Transcriptional analysis of metastatic hormone-naïve prostate cancer primary tumour biopsies reveals a relevant role for SOX11 in prostate cancer cell dissemination [scRNA-Seq]

| PRJNA1116143 | ENA

Transcriptional analysis of metastatic hormone-naïve prostate cancer primary tumour biopsies reveals a relevant role for SOX11 in prostate cancer cell dissemination [Validation dataset]

| PRJNA1116141 | ENA

| PRJNA1117040 | ENA

The transcriptional landscape of metastatic hormone-naïve prostate cancer

Project description:Background Metastatic hormone-naïve prostate cancer (mHNPC) is an infrequent form of this tumour type that is characterized by metastasis at the time of diagnosis and accounts for 50% of prostate cancer-related deaths. Despite the extensive characterization of localized and metastatic castration resistant prostate cancer (mCRPC), the molecular characteristics of mHNPC remain largely unexplored. Results Here we provide the first extensive transcriptomics characterization of mHNPC. We generated discovery and validation bulk and single-cell RNA-Seq datasets and performed integrative computational analysis in combination with experimental studies. Our results provide unprecedented evidence of the distinctive transcriptional profile of mHNPC and identify stroma remodelling as a predominant feature of these tumours. Importantly, we discover a central role for the transcription factor SOX11 in triggering a heterotypic communication that is associated to the acquisition of metastatic properties. Conclusions Our study will constitute an invaluable resource for a profound understanding of mHNPC that can influence patient management.

2025-05-07 | PXD063665 | Pride

Expression profiling of prostate cancer biopsies.

Project description:This work was conducted to identify shared and specific target genes of different ETS transcription factor rearrangements in prostate cancer. Potential target genes were identified by differential gene expression analysis of primary tumor samples with ETS rearrangements, and validated by ETS silencing in prostate cancer cell lines.

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SOX11-SMARCA4 Complex Drives Oncogenic Gene Regulation in Mantle Cell Lymphoma

Project description:SOX11 pioneer transcription factor is aberrantly expressed, it has an oncogenic role and its overexpression associates with worse prognosis in patients with mantle cell lymphomas (MCL). Using a proximity labeling (BioID2)/Mass Spectrometry-based proteomic strategyies, we identified SMARCA4, the central catalytic subunit of the SWI/SNF chromatin-remodeling complex, as one of the most significant SOX11-specific interacting proteins. SMARCA4 expression is directly regulated by SOX11, and its upregulation is associated with worse overall survival in patients with MCL, independently of other high-risk factors. Integration of global DNA-binding and transcriptomic profiles revealed that SOX11 and SMARCA4 share 60% specific peaks, predominantly in promoter regions. Disruption of SOX11:SMARCA4 interaction via SOX11 knockout or SMARCA4 PROTAC-degradation significantly reduced co-occupancy and co-targeted gene expression, including key BCR signaling pathway components. Our results suggest that SOX11:SMARCA4 complex binds to common regulatory sequences enabling the accession to chromatin and transcriptomic regulation of key oncogenic pathways for the development of MCL pathogenesis.

2025-08-04 | PXD051143 | Pride

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