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Castration-induced SPARC down-regulation in stroma cells drives neuroendocrine differentiation of prostate cancer

ABSTRACT: Castration-induced SPARC down-regulation in stroma cells drives neuroendocrine differentiation of prostate cancer

PROVIDER: PRJNA656516 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12429729.fastq.gz	Fastqsanger.gz
	SRR12429730.fastq.gz	Fastqsanger.gz
	SRR12429731.fastq.gz	Fastqsanger.gz
	SRR12429732.fastq.gz	Fastqsanger.gz
	SRR12429733.fastq.gz	Fastqsanger.gz

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Castration-induced SPARC down-regulation in stroma cells drives neuroendocrine differentiation of prostate cancer

Project description:Fatal neuroendocrine (NE) prostate cancer evolves from castration-resistant adenocarcinoma as a mechanism of resistance to androgen deprivation/anti androgen receptor therapies. Evidence suggests the microenvironment as a possible source of soluble factors mediating neuroendocrine differentiation (NED), but molecular mechanisms are unknown. Using a transgenic mouse model we show that upon castration tumor cells up-regulate GRP78, which triggers a cascade leading to down-regulation of the matricellular protein SPARC in the nearby stroma. SPARC loss allows stroma cells to release IL-6, a known inducer of NED. A drug targeting GRP78 blocks NED in castrated mice. These events find correlation in prostate cancer patients developing focal NED after androgen deprivation therapies. Our results candidate SPARC and GRP78 for diagnostic and therapeutic purpose, respectively.

2021-07-30 | GSE156033 | GEO

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Project description:In this dataset we show transcriptional profiles derived from adenocarcinoma or incipient neuroendocrine prostate cancer (NEPC) derived from TRAMP or SPARC-deficient TRAMP mice respectively. Genetic ablation of SPARC rendered prostate cancer cells to be prone to NEPC differentiation.

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4T1 breast cancer cells: SPARC knock down vs. Control

Project description:Comparative analysis of the transcriptome of 4T1 cells stably transduced with a lentiviral vector expressing a siRNA against murine SPARC (4T1-C18) with 4T1 control cells stably transduced with a lentiviral vector expressing a scramble sequence (4T1-SCR). Two-condition experiment, 4T1-C18 vs. 4T1-SCR cells. Biological replicates: 4 SPARC knock down, 4 control, independently grown in vitro and harvested. One replicate per array. Microarrays were hybridized in three different days.

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4T1 breast cancer cells: SPARC knock down vs. Control

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Expression data from Min6 cells overexpressing control or SPARC adenovirus

Project description:SPARC-deficient mice have been shown to exhibit impaired glucose tolerance and insulin secretion, but the underlying mechanism remains unknown. We used microarrays to detail the global programme of gene expression and identified distinct classes of up-regulated and down-regulated genes changed by overexpressing SPARC.

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Single-cell analysis of castration-resistant prostate cancers to identify potential biomarkers for diagnosis and prognosis of neuroendocrine prostate cancer

Project description:The high heterogeneity and low percentage of neuroendocrine cells in prostate cancer limit the utility of traditional bulk RNA sequencing and even single-cell RNA sequencing to find better biomarkers for early diagnosis and stratification. Re-clustering of specific cell-type holds great promise for identification of intra-cell-type heterogeneity. However, this has not yet been used in studying neuroendocrine prostate cancer heterogeneity. Neuroendocrine cluster(s) were individually identified in each castration-resistant prostate cancer specimen and combined for trajectory analysis. Three neuroendocrine states were identified. Neuroendocrine state 2 with the highest AR score was considered the initial starting state of neuroendocrine transdifferentiation. State 1 and state 3 with distinct high neuroendocrine scores and marker genes enriched in N-Myc and REST target genes, respectively, were considered as two different types of neuroendocrine differentiated cancer cells. These two states contained distinct groups of prostate cancer biomarkers and a strong distinguishing ability of normal versus cancerous prostate across different pathological grading was found in the N-Myc-associated state. Our data highlight the central role of N-Myc and REST in mediating lineage plasticity and classifying neuroendocrine phenotypes.

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Project description:Assessment of mesenteric fibrosis (MF) presence and severity in small-intestinal neuroendocrine tumors (SI-NETs) remains a diagnostic challenge. To explore possible biomarkers for MF presence, a proteomic analysis was performed of the tumor and stroma compartment of primary SI-NETs and paired mesenteric metastasis.

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Project description:Background: Neuroendocrine prostate cancer (NEPC), a lethal subset of prostate cancer, is characterized by loss of AR signaling and resulting resistance to AR-targeted therapy during neuroendocrine transdifferentiation, for which the molecular mechanisms remain unclear. Here, we report that SRY-Box transcription factor 4 (SOX4) is upregulated in NEPC, which induces neuroendocrine markers, neuroendocrine cell morphology, and NEPC cell aggressive behavior. Methods: To understand the function of SOX4 in the development and progression of NEPC, we detected malignancy characterization after over-expression or knock-down of SOX4 in prostate cancer cells. Xenograft tumors representing NEPC subtypes were analyzed by pathologists. Protein expression profiles were validated in patient tumor tissue. Diagnoses were complemented by transcriptome sequencing and ATAC sequencing of specific cell lines and public clinical datasets. Results: SOX4 expression was significantly elevated in NEPC. Activating SOX4 in non-NEPC cells induced NE transdifferentiation, while silencing it in NEPC cells impeded NEPC progression. SOX4 promote neuroendocrine characteristics by inducing PCK2-mediated metabolism changing. Conclusions: Elevated SOX4 drives NE transdifferentiation in PCa via PCK2-mediated . Altogether, these findings highlight SOX4 as a novel molecule to drive NEPC progression and suggest that it might be a potential therapeutic target for NEPC.

2024-03-31 | GSE261370 | GEO

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