Methodological aspects of the molecular and histological study of prostate cancer: Focus on PTEN

Ugalde-Olano, Aitziber; Egia, Ainara; Fernández-Ruiz, Sonia; Loizaga-Iriarte, Ana; Zúñiga-García, Patricia; García, Stéphane; Royo, Félix; Lacasa-Viscasillas, Isabel; Castro, Erika; Cortazar, Ana R.; Zabala-Letona, Amaia; Martín-Martín, Natalia; Arruabarrena-Aristorena, Amaia; Torrano, Verónica; Valcárcel-Jiménez, Lorea; Sánchez-Mosquera, Pilar; Caro‐Maldonado, Alfredo; González-Tampán, J.; Cachi-Fuentes, Guido; Bilbao, Elena; Montero, Rocío Sánchez; Fernández, Sara; Arrieta, Edurne; Zorroza, Kerman; Castillo-Martín, Mireia; Serra, Violeta; Salazar, E.; Macías-Cámara, Nuria; Tabernero, Josep; Baselga, J.; Cordon‐Cardo, Carlos; Aransay, Ana M.; Villar, Amaia Del; Iovanna, Juan; Falcón‐Pérez, Juan Manuel; Unda, Miguel; Bilbao, Roberto; Carracedo, Arkaitz

doi:10.1016/j.ymeth.2015.02.005

Cited by 17 publications

(22 citation statements)

References 28 publications

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“…As a first approach, we analyzed the physical characteristics of uEVs from patients with BPH and PCa by comparing more than 23–30 independent preparations from each group ( Supplementry Table S1 ). In order to validate the ultracentrifugation procedure [ 16 ] for isolation of uEVs, the presence of double membrane vesicles by cryo-electron microscopy (Figure 1A ) and EV markers by western blot [ 28 ] was confirmed ( Supplementary Figure S1 ). We next analyzed uEV size and number in urine of BPH and PCa patients.…”

Section: Resultsmentioning

confidence: 99%

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Transcriptomic profiling of urine extracellular vesicles reveals alterations of CDH3 in prostate cancer

et al. 2016

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Extracellular vesicles (EV) are emerging structures with promising properties for intercellular communication. In addition, the characterization of EV in biofluids is an attractive source of non-invasive diagnostic, prognostic and predictive biomarkers. Here we show that urinary EV (uEV) from prostate cancer (PCa) patients exhibit genuine and differential physical and biological properties compared to benign prostate hyperplasia (BPH). Importantly, transcriptomics characterization of uEVs led us to define the decreased abundance of Cadherin 3, type 1 (CDH3) transcript in uEV from PCa patients. Tissue and cell line analysis strongly suggested that the status of CDH3 in uEVs is a distal reflection of changes in the expression of this cadherin in the prostate tumor. CDH3 was negatively regulated at the genomic, transcriptional, and epigenetic level in PCa. Our results reveal that uEVs could represent a non-invasive tool to inform about the molecular alterations in PCa.

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Section: Resultsmentioning

confidence: 99%

“…From this analysis, we selected two transcripts, Eukaryotic Elongation Factor 1A1 (EEF1A1) and Ribosomal Protein L6 (RPL6), that we monitored in subsequent studies. In addition, we also included Glyceraldehyde Phosphate Dehydrogenase (GAPDH) as a housekeeping gene supported by prior studies of our group [ 16 ].…”

Section: Resultsmentioning

confidence: 99%

Transcriptomic profiling of urine extracellular vesicles reveals alterations of CDH3 in prostate cancer

et al. 2016

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“…We evaluated PPARD mRNA (11 benign prostate hyperplasia and 16 primary prostate cancer tissue extracts harvested following the guidelines reported; ref. 20) in human specimens. The results revealed a significant downregulation of PPARD in cancerous tissues compared with benign disease (Fig.…”

Section: Ppard Inhibits Prostate Cancer Aggressivenessmentioning

confidence: 98%

PPARδ Elicits Ligand-Independent Repression of Trefoil Factor Family to Limit Prostate Cancer Growth

et al. 2018

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The nuclear receptor PPAR-β/δ (PPARD) has essential roles in fatty acid catabolism and energy homeostasis as well as cell differentiation, inflammation, and metabolism. However, its contributions to tumorigenesis are uncertain and have been disputed. Here, we provide evidence of tumor suppressive activity of PPARD in prostate cancer through a noncanonical and ligand-independent pathway. PPARD was downregulated in prostate cancer specimens. In murine prostate epithelium, PPARD gene deletion resulted in increased cellularity. Genetic modulation of PPARD in human prostate cancer cell lines validated the tumor suppressive activity of this gene and Mechanistically, PPARD exerted its activity in a DNA binding-dependent and ligand-independent manner. We identified a novel set of genes repressed by PPARD that failed to respond to ligand-mediated activation. Among these genes, we observed robust regulation of the secretory trefoil factor family (TFF) members, including a causal and correlative association of TFF1 with prostate cancer biology and in patient specimens. Overall, our results illuminate the oncosuppressive function of PPARD and understanding of the pathogenic molecular pathways elicited by this nuclear receptor. These findings challenge the presumption that the function of the nuclear receptor PPARβ/δ in cancer is dictated by ligand-mediated activation. .

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“…RNA was extracted using NucleoSpin RNA isolation kit from Macherey-Nagel (ref: 740955.240C). For xenograft samples, a TRIzol-based implementation of the NucleoSpin RNA isolation kit protocol was used as reported (24). For all cases, 1 mg of total RNA was used for cDNA synthesis using qScript cDNA Supermix from Quanta (ref: 95048).…”

Section: Cellular and Molecular Assaysmentioning

confidence: 99%

PGC1α Suppresses Prostate Cancer Cell Invasion through ERRα Transcriptional Control

et al. 2019

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The PPARg coactivator 1 alpha (PGC1a) is a prostate tumor suppressor that controls the balance between anabolism and catabolism. PGC1A downregulation in prostate cancer is causally associated with the development of metastasis. Here we show that the transcriptional complex formed by PGC1a and estrogen-related receptor 1 alpha (ERRa) controls the aggressive properties of prostate cancer cells. PGC1a expression significantly decreased migration and invasion of various prostate cancer cell lines. This phenotype was consistent with remarkable cytoskeletal remodeling and inhibition of integrin alpha 1 and beta 4 expression, both in vitro and in vivo. CRISPR/ Cas9-based deletion of ERRa suppressed PGC1a regulation of cytoskeletal organization and invasiveness. Mechanistically, PGC1a expression decreased MYC levels and activity prior to inhibition of invasiveness. In addition, PGC1a and ERRa associated at the MYC promoter, supporting the inhibitory activity PGC1a. The inverse correlation between PGC1a-ERRa activity and MYC levels was corroborated in multiple prostate cancer datasets. Altogether, these results support that PGC1a-ERRa functions as a tumor-suppressive transcriptional complex through the regulation of metabolic and signaling events. Significance: These findings describe how downregulation of the prostate tumor suppressor PGC1 drives invasiveness and migration of prostate cancer cells.

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Methodological aspects of the molecular and histological study of prostate cancer: Focus on PTEN

Cited by 17 publications

References 28 publications

Transcriptomic profiling of urine extracellular vesicles reveals alterations of CDH3 in prostate cancer

Transcriptomic profiling of urine extracellular vesicles reveals alterations of CDH3 in prostate cancer

PPARδ Elicits Ligand-Independent Repression of Trefoil Factor Family to Limit Prostate Cancer Growth

PGC1α Suppresses Prostate Cancer Cell Invasion through ERRα Transcriptional Control

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