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Single nuclear RNA sequencing and 10X spatial transcriptomic profiling of murine tumors initiated by transplantation of engineered prostate organoids [visium]

ABSTRACT: Single-nuclear RNA-sequencing of murine organoid transplant-derived prostate tumors. Purpose: To identify differences in cell composition in murine prostatic tumors and to generate a reference dataset of all major cell types present in mouse prostate tumors Results: We recovered 4,872 cells with a median of 7055.5 UMIs per cell. Conclusions: snRNASeq reveals heterogeneity within neuroendocrine prostate cancer compartment, dominated by an Ascl1+ expression profile with mixed luminal lineage marker genes. snRNASeq recovers all the major epithelial, immune, and stromal cell types in prostate tumors. Spatial transcriptomic profiling of murine prostate tumors. Purpose: To spatially map the major cell types in the mouse prostatic tumors and identify spatially distinct neuroendocrine tumor compartments. Distinct tumor microenvironments were also used for identification of cell:cell signaling axes distributed between the histological subtypes. Conclusions: Spatial transcriptomic profiling of the mouse prostate reveals all major cell types and allows for cell:cell signaling analyses upon integration with our matching snRNA-Seq data

ORGANISM(S): Mus musculus

PROVIDER: GSE246762 | GEO | 2024/08/02

REPOSITORIES: GEO

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Single nuclear RNA sequencing and 10X spatial transcriptomic profiling of murine tumors initiated by transplantation of engineered prostate organoids [snRNA-seq]

Project description:Single-nuclear RNA-sequencing of murine organoid transplant-derived prostate tumors. Purpose: To identify differences in cell composition in murine prostatic tumors and to generate a reference dataset of all major cell types present in mouse prostate tumors Results: We recovered 4,872 cells with a median of 7055.5 UMIs per cell. Conclusions: snRNASeq reveals heterogeneity within neuroendocrine prostate cancer compartment, dominated by an Ascl1+ expression profile with mixed luminal lineage marker genes. snRNASeq recovers all the major epithelial, immune, and stromal cell types in prostate tumors. Spatial transcriptomic profiling of murine prostate tumors. Purpose: To spatially map the major cell types in the mouse prostatic tumors and identify spatially distinct neuroendocrine tumor compartments. Distinct tumor microenvironments were also used for identification of cell:cell signaling axes distributed between the histological subtypes. Conclusions: Spatial transcriptomic profiling of the mouse prostate reveals all major cell types and allows for cell:cell signaling analyses upon integration with our matching snRNA-Seq data

2024-08-02 | GSE246768 | GEO

Bulk RNA-sequencing of mouse prostate tumors initiated by transplantation of engineered organoids.

Project description:Purpose: Profile global expression of prostatic tumors to compare with published datasets. Methods: Prostate tumors were flash frozen followed by processed for total RNA using the RNeasy kit (Qiagen). Samples were submitted for polyA library preparation and bulk RNA-sequencing. Conclusions: Global gene expression profiling and comparison of prostate tumor genotypes suggests differential enrichment of neuroendocrine signatures that match established human neuroendocrine prostate cancer expression signatures.

2024-08-02 | GSE246251 | GEO

LOSS OF THE TUMOR SUPPRESSOR, TP53, ENHANCES THE ANDROGEN RECEPTOR MEDIATED ONCOGENIC TRANSFORMATION AND TUMOR DEVELOPMENT IN THE MOUSE PROSTATE

Project description:Androgen signaling is essential for prostate tumorigenesis. The tumor suppressor p53 has been implicated in prostate cancer progression. Recent genome analysis of human prostate cancers demonstrated that both AR gene amplification and TP53 deletion are frequently altered in advanced prostate cancer. However, the biological role of these dual genetic alterations in prostate tumorigenesis is largely unknown. In addition, there are no biologically relevant models that can be used to assess these genetic abnormalities in the prostate. Here, we report a novel mouse model, in which elevated transgenic AR expression and Trp53 deletion occur simultaneously in mouse prostatic epithelium to mimic what happens in human prostate cancer cells. These compound mice developed an earlier onset of high-grade prostatic intraepithelial neoplasia and accelerated prostate tumors. Histological analysis showed pathological lesions resembling prostatic sarcomatoid and basaloid carcinomas with massive squamous differentiation in the above compound mice. RNA-sequencing analyses showed a robust enrichment of the signature genes for human prostatic basal cell carcinomas in the above prostate tumors. The Master Regulator Analysis further identified SOX2 as a transcriptional regulator in prostatic basal cell tumors. Elevated expression of SOX2 and its downstream target genes were detected in prostatic tumors of the compound mice. Chromatin immunoprecipitation analyses implicate a co-regulatory role of AR and SOX2 in the expression of prostatic basal cell signature genes. These results demonstrate a novel mechanism underlying elevated AR expression and Trp53 deletion induced prostate cancer cell trans-differentiation, aggressiveness, and progression.

2019-04-03 | GSE129243 | GEO

Distinctive gene expression of prostatic stromal cells cultured from diseased versus normal tissues

Project description:To obtain a comprehensive view of the transcriptional programs in prostatic stromal cells of different histological/pathological origin, we profiled 18 adult human stromal cell cultures from normal transition zone (TZ), normal peripheral zone (PZ), benign prostatic hyperplasia (BPH), and prostate cancer (CA) using cDNA microarrays. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set

2006-11-10 | GSE6250 | GEO

RET Kinase Inhibition in Neuroendocrine Prostate Cancer, part 2

Project description:Increased treatment of metastatic castration resistant prostate cancer (mCRPC) with second-generation anti-androgen therapies (ADT) has coincided with a greater incidence of lethal, aggressive variant prostate cancer (AVPC) tumors that have lost androgen receptor (AR) signaling. AVPC tumors may also express neuroendocrine markers, termed neuroendocrine prostate cancer (NEPC). Recent evidence suggests kinase signaling may be an important driver of NEPC. To identify targetable kinases in NEPC, we performed global phosphoproteomics comparing AR-negative to AR-positive prostate cancer cell lines and identified multiple altered signaling pathways, including enrichment of RET kinase activity in the AR-negative cell lines. Clinical NEPC and NEPC patient derived xenografts displayed upregulated RET transcript and RET pathway activity. Pharmacologically inhibiting RET kinase in NEPC models dramatically reduced tumor growth and cell viability in mouse and human NEPC models. Our results suggest that targeting RET in NEPC tumors with high RET expression may be a novel treatment option.

2020-05-29 | PXD012971 | Pride

RET Kinase Inhibition in Neuroendocrine Prostate Cancer, part 1

2020-05-29 | PXD012970 | Pride

Genetic deletion of osteopontin in TRAMP mice enhances the growth of aggressive prostate cancer with feature of human neuroendocrine tumors

Project description:Osteopontin (OPN) is a secreted glycoprotein, belonging to the non-structural extracellular matrix (ECM), and its over expression in human prostate cancer cells has been associated with disease progression, androgen independence and metastases. Nevertheless the pathophysiology of OPN in prostate tumorigenesis has never been studied. We crossed TRansgenic Adenocarcinoma of the Mouse Prostate (TRAMP) mice with OPN deficient (OPN-/-) mice and followed tumor onset and progression in these double mutants. Ultrasound examination detected the early onset of a spherical homogeneous tumor in about 60% of OPN-/- TRAMP mice that seldom occurs in parental TRAMP mice. Histology and immunohistochemistry characterized these tumors for being Tag positive but negative for AR, highly proliferative and endowed of neuroendocrine (NE) features. Gene expression profiling showed up-regulation of genes involved in tumor progression, cell cycle and neuronal differentiation in OPN-deficient versus -sufficient TRAMP tumors. Down-regulated genes included key genes of TGFï?¢ pathway, and a role for TGFï?¢ in NE differentiation of prostate cancer was also confirmed at the protein level. Furthermore, NE genes and particularly those characterizing early prostatic lesions of OPN-deficient mice were found to correlate with those of human NE tumours. These data underscore a novel role of OPN at early stages of prostate cancer growth, protecting against the development of aggressive NE tumors. Total RNA obtained from prostate tumors from 18 and 30 weeks old TRAMP mice, compared to RNA extracted from prostate tumors and prostate tissue from Osteopontin-deleted TRAMP mice

2016-01-20 | E-GEOD-69903 | biostudies-arrayexpress

Genome-wide characterization of REST binding regions in LNCaP prostate cancer cells

Project description:Transcriptional regulator REST plays a key role in repressing neuronal specific genes in prostate cancer and other non-neuronal tissues. Moreover, loss of REST is observed in neuroendocrine prostate tumors. Here, we use ChIP-seq analysis to study genome–wide REST occupied regions in the prostate cancer cell line, LNCaP. REST occupied regions were then correlated to gene expression changes occurring between prostate adenocarcinoma and neuroendocrine prostate tumors in vivo.

2019-09-03 | GSE119385 | GEO

Niacin restriction with NAMPT-inhibition is synthetic lethal to neuroendocrine carcinoma (Mouse NAD targeted time-course)

Project description:NAMPT plays a major role in NAD biosynthesis in many cancers and is an attractive potential cancer target. However, factors dictating therapeutic efficacy of NAMPT inhibitors (NAMPTi) are unclear. We report that neuroendocrine phenotypes predict lung and prostate carcinoma vulnerability to NAMPTi, and that NAMPTi therapy against those cancers is enhanced by dietary modification. Neuroendocrine differentiation of tumor cells was associated with down-regulation of genes relevant to QPRT-dependent de novo NAD synthesis, promoting NAMPTi susceptibility in vitro. We also found that circulating nicotinic acid riboside (NAR), a non-canonical niacin absent in culture media, antagonizes NAMPTi efficacy as it fuels NAMPT-independent but NMRK1-dependent NAD synthesis in tumors. In mouse transplantation models, depleting blood NAR by nutritional or genetic manipulations was synthetic lethal to tumors when combined with NAMPTi. Our findings provide a rationale for simultaneous targeting of NAR metabolism and NAMPT therapeutically in neuroendocrine carcinoma. Mouse NAD targeted time-course is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS7253' rel='noopener noreferrer' target='_blank'>MTBLS7253</a>.Cell NAMPTi treatment is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS7251' rel='noopener noreferrer' target='_blank'>MTBLS7251</a>.Mouse NAMPT targeted therapy is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS7252' rel='noopener noreferrer' target='_blank'>MTBLS7252</a>.

2023-10-10 | MTBLS7253 | MetaboLights

Niacin restriction with NAMPT-inhibition is synthetic lethal to neuroendocrine carcinoma (Cell NAMPTi treatment)

Project description:NAMPT plays a major role in NAD biosynthesis in many cancers and is an attractive potential cancer target. However, factors dictating therapeutic efficacy of NAMPT inhibitors (NAMPTi) are unclear. We report that neuroendocrine phenotypes predict lung and prostate carcinoma vulnerability to NAMPTi, and that NAMPTi therapy against those cancers is enhanced by dietary modification. Neuroendocrine differentiation of tumor cells was associated with down-regulation of genes relevant to QPRT-dependent de novo NAD synthesis, promoting NAMPTi susceptibility in vitro. We also found that circulating nicotinic acid riboside (NAR), a non-canonical niacin absent in culture media, antagonizes NAMPTi efficacy as it fuels NAMPT-independent but NMRK1-dependent NAD synthesis in tumors. In mouse transplantation models, depleting blood NAR by nutritional or genetic manipulations was synthetic lethal to tumors when combined with NAMPTi. Our findings provide a rationale for simultaneous targeting of NAR metabolism and NAMPT therapeutically in neuroendocrine carcinoma. Cell NAMPTi treatment is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS7251' rel='noopener noreferrer' target='_blank'>MTBLS7251</a>.Mouse NAMPT targeted therapy is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS7252' rel='noopener noreferrer' target='_blank'>MTBLS7252</a>.Mouse NAD targeted time-course is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS7253' rel='noopener noreferrer' target='_blank'>MTBLS7253</a>.

2023-10-10 | MTBLS7251 | MetaboLights

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