ScRNA of either HSPC or CRPC Ptenpc-/- mouse prostate cancers
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE272965 | GEO | 2024/08/21
REPOSITORIES: GEO
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Project description:PTEN is one of the most altered tumor suppressor genes in human prostate cancer (PCa). Prostate specific-Pten-deficient mouse models develop prostate cancer eventually progressing to castration-resistant prostate cancer (CRPC), also due to alterations of the tumor immune infiltrate. By using single-cell RNA-seq, we report the identification of a subset of CD84+; CD11b+; Ly6G+; Ly6Clow immunosuppressive neutrophils that secreted the coagulation factor X (FX) into the prostate TME to directly promote PCa growth.
2024-08-21 | GSE272967 | GEO
Project description:scRNA of either HSPC or CRPC Ptenpc-/- mouse prostate cancers
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Project description:PB-Cre/Pten/Smad4 is a transgenic mouse model of metastatic prostate adenocarcinoma (PMID: 21289624). To study the transcriptomic alterations associated with castration-resistant prostate cancer (CRPC), the PB-Cre/Pten/Smad4 males with established prostate cancer were treated with surgical castration followed by enzalutamide-admixed diet. After about 4 weeks, dorsolateral prostate (DLP) lobes of treatment-naïve prostate tumors (N=2) and CRPC tumors (N=3) were harvested and extracted for RNA purification and microarray profiling. To further study the transcriptomic changes associated with lung metastases of the PB-Cre/Pten/Smad4/mTmG CRPC model, the PB-Cre/Pten/Smad4 males with established prostate cancer were treated with surgical castration followed by enzalutamide-admixed diet. About 3 months later, from one mouse anterior prostate (AP), dorsolateral prostate (DLP), ventral prostate (VP) and GFP+ lung metastasis nodules were each harvested for RNA purification and microarray profiling.
2020-12-18 | GSE163420 | GEO
Project description:Identifying biological change from hormone-naive prostate cancer to CRPC is a major clinical challenge for developing therapeutic agents. Although the pathways that lead to CRPC are not fully understood, recent evidence demonstrates that androgen signaling is often maintained through varied mechanisms. Here, we investigated PCa tissues at each stage of progression from benign prostatic hyperplasia (BPH) to CRPC based on quantitative proteomic technology, including tissues after ADT therapy. MS-based quantitative proteomics approach based on 6-plex TMT (126-131) was performed in patient tissues from T2G2 to CRPC, and benign prostatic hyperplasia (BPH) patient tissues were used as a control. We analyzed the peptide samples using two types of high resolution and accuracy mass spectrometers as LTQ orbitrap velos and Q-exactive mass spectrometer. In total, 4,768 proteins were identified in this study, among which 4,069 proteins were quantified in the combined prostate cancer tissues. Among the quantified proteins, DEPs were 865 (21.2%), those with a quantitative ratio greater than 2 were considered as upregulated, whereas those with a quantitative ratio of less than 0.5 as downregulated. Based on quantitative protein results, we performed systematic bioinformatics analysis including GO, Interpro, KEGG pathway, functional enrichment-based cluster analysis on DEPs. Finally, we found that 15 proteins including FOXA1 and HMGN1-3 between T3G3, T3GX, and CRPC were increased despite ADT treatment. Among all target, we verified increased level of FOXA1 and HMGN1-3 in CRPC by immunoblotting and indirect ELISA. In summary, we provides intracellular mechanical changes on PCa tissues according to treatment before and after ADT by mean of regulating ADT treatment. In addition, this results were identified through bioinformatics analysis, and those were suggested as potential CRPC-related factors.
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Project description:Gene expression data from Agilent-014850 4x44K human expression array for CRPC Prostate Cancer study with Xenograph data. RNA was isolated using the mirVana total RNA protocol (part #AM1560, Ambion, Austin, TX). RNA integrity was verified using a 2100 Bioanalyzer (part #G2938A) with nano chips (parts #5067-15101 and #G4411B; Agilent Technologies, Alto, CA). RNA concentrations were determined using a Nanodrop spectrophotometer (Thermo Scientific, Wilmington, DE). Tumor messenger RNA expression was assessed using a human whole-genome oligo TMA kit from Agilent (prod #G4112F) according to the manufacturer’s protocol and as described previously. In the Characteristics field, we have the notation like "Pt Dxed in 2001; hormone Tx; chemo Tx 2002; HRPC by 2002". That means the patient was admitted in 2001, did hormone and chemo treatment in 2002, and HRPC 2002. They are standard prostate cancer treatments.
2011-12-31 | E-GEOD-33277 | biostudies-arrayexpress
Project description:To investigate if there is a difference of N6-methyladenosine(m6A) modification between castration-resistant prostate cancer (CRPC) and castration-sensitive prostate cancer (CSPC), we collected 30 specimens, including 15 CRPC and 15 CSPC, to perform RNA-seq and MeRIP-seq. All specimens were postoperative tissues and each 5 CRPC or CSPC specimens were mixed into 1 sample to meet the RNA dosage of RNA-seq and MeRIP-seq.
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Project description:Gene expression data from Agilent-014850 4x44K human expression array for CRPC Prostate Cancer study with Xenograph data.
2011-12-31 | GSE33277 | GEO
Project description:Exome sequencing of 10 biopsies from the same CRPC tumor
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Project description:Advanced prostate cancer (PCa) is a clinical challenge as this state of the disease lacks of curative therapeutic. We exploited human datasets as well as mouse models to decipher mechanisms able to constrain cancer evolution in response to genetic alteration that occurs in PCa. Careful analysis of transcriptomic signature of various PCa datasets reveals activation of the LXR target gene signature. This LXR signature is tightly correlated to PTEN-loss in human. Causal LXR deregulation has been confirmed using prostate mouse carcinomas from Pten-null mutant. Protective role of LXR has been demonstrated by their deletions in a Pten-null context in mouse prostate, thus results in an increase of PCa invasiveness and metastatic dissemination. PTEN deletion governs LXR transcriptional activity through deregulation of cholesterol de novo synthesis that leads to the accumulation of LXR ligands. According to these observations, pharmacological inhibition of cholesterol biosynthesis using statins abolishes LXR target gene expression in response to PTEN-loss. LXR deletion triggers an increased in the epithelial mesenchymal transition process and matrix metalloproteinase accumulations that could explain metastatic spreading. This work highlights LXRs as metabolic sensors that act as gatekeeper able to constrain carcinoma progression.
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