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Snai2-mediated upregulation of NADSYN1 promotes bladder cancer progression by interacting with PHB

ABSTRACT: Prohibitin (PHB) plays a significant role in cancer processes whereas its mechanism in bladder cancer (BC) aggressiveness is not fully understood. This study aimed to investigate the role of PHB in BC aggressiveness. The study employed a range of in vivo and in vitro assays to elucidate the interaction between PHB-NADSYN1 and its underlying function in BC progression. We found that PHB was upregulated in muscle-invasive bladder cancer tissues, and bound to NADSYN1 mRNA in BC tissues more than in adjacent normal tissues. NADSYN1 and PHB were upregulated and positively correlated both in BC tissues and cell lines. We further revealed that deleting NADSYN1 prevented PHB-mediated cell invasiveness of BC in vivo and in vitro. PHB could directly bind to NADSYN1 mRNA, and it was found that the PHB domain was responsible for the PHB-NADSYN1 interaction. Depletion of NADSYN1 expression significantly decreased the protein level of PHB. In addition, Snai2 positively correlated with NADSYN1 and depletion or mutation of Snai2 binding sites inhibited NADSYN1-PHB-mediated BC progression. The study highlights a novel Snai2-NADSYN1-PHB mechanism in BC progression and indicates that PHB and NADSYN1 could serve as a therapeutic target for BC

ORGANISM(S): Homo sapiens

PROVIDER: GSE243441 | GEO | 2024/01/24

REPOSITORIES: GEO

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Snai2-mediated upregulation of NADSYN1 promotes bladder cancer progression by interacting with PHB

Project description:Snai2-mediated upregulation of NADSYN1 promotes bladder cancer progression by interacting with PHB

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PHB Acts as a Member of the HIRA Complex to Control an Epigenetic and Metabolic Circuitry

Project description:Cellular metabolism and chromatin landscape both contribute to cell fate determination. However, their interplay remains poorly understood. Here we show that Prohibitin (PHB), an evolutionarily conserved protein, involves in a histone variant H3.3 chaperon HIRA complex-dependent epigenetic and metabolic circuitry to maintain the identity of human embryonic stem cells (hESCs). We found that silencing of PHB triggers hESC differentiation with concomitant enhancements of histone 3 (H3) lysine (K) methyl modifications as a result of the reduced production of Î±-ketoglutarate (Î±-KG), a metabolite required for activities of many dioxygenase and in turn chromatin structure1,2. Mechanistically, PHB acts as a functional member of the HIRA complex3,4. Resembling PHB deficiency, loss of HIRA in hESCs leads to massive differentiation and aberrant histone modifications, although it was previously found not to disrupt the self-renewal in mouse ESCs (mESCs)5. Genome-wide H3.3 ChIP- sequence analyses indicate that reduction of H3.3 deposition caused by PHB knock down is extremely similar to that induced by HIRA knock down. Specifically, silencing either HIRA or PHB leads to repressive chromatin characters at promoters of pluripotency genes and isocitrate dehydrogenases (IDHs), the enzyme responsible for Î±-KG production, but active chromatin features at promoters of developmental genes, paralleling to transcript levels of these genes. Our results identify PHB as an essential factor not only for hESC self-renewal but also for the proper function of the HIRA complex, linking the HIRA complex-dependent H3.3 deposition to the production of a critical metabolite required for shaping chromatin structure, and demonstrating the importance of the interplay between epigenetic state and metabolic regulation in cell fate determination. Examination of H3.3 deposition in NT, PHB, and HIRA siRNA treated hESCs respectively.

2016-08-11 | E-GEOD-72143 | biostudies-arrayexpress

PHB Acts as a Member of the HIRA Complex to Control an Epigenetic and Metabolic Circuitry

Project description:Cellular metabolism and chromatin landscape both contribute to cell fate determination. However, their interplay remains poorly understood. Here we show that Prohibitin (PHB), an evolutionarily conserved protein, involves in a histone variant H3.3 chaperon HIRA complex-dependent epigenetic and metabolic circuitry to maintain the identity of human embryonic stem cells (hESCs). We found that silencing of PHB triggers hESC differentiation with concomitant enhancements of histone 3 (H3) lysine (K) methyl modifications as a result of the reduced production of α-ketoglutarate (α-KG), a metabolite required for activities of many dioxygenase and in turn chromatin structure1,2. Mechanistically, PHB acts as a functional member of the HIRA complex3,4. Resembling PHB deficiency, loss of HIRA in hESCs leads to massive differentiation and aberrant histone modifications, although it was previously found not to disrupt the self-renewal in mouse ESCs (mESCs)5. Genome-wide H3.3 ChIP- sequence analyses indicate that reduction of H3.3 deposition caused by PHB knock down is extremely similar to that induced by HIRA knock down. Specifically, silencing either HIRA or PHB leads to repressive chromatin characters at promoters of pluripotency genes and isocitrate dehydrogenases (IDHs), the enzyme responsible for α-KG production, but active chromatin features at promoters of developmental genes, paralleling to transcript levels of these genes. Our results identify PHB as an essential factor not only for hESC self-renewal but also for the proper function of the HIRA complex, linking the HIRA complex-dependent H3.3 deposition to the production of a critical metabolite required for shaping chromatin structure, and demonstrating the importance of the interplay between epigenetic state and metabolic regulation in cell fate determination.

2016-08-11 | GSE72143 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of PHB-knockdown and PHB-knockout Spermatocytes Transcriptomes

Project description:We analyzed the transcriptomic differences of cultured mouse spermatocytes (GC2 cells) stably transfected with PHB-targeting shRNA (called PHB KD GC2) from those with a control shRNA (called Ctrl GC2). Furthermore, we also analyzed the difference in the transcriptomes of spermatocytes between Phb conditional knock-out and control mice.

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Project description:The biodegradable polymer poly-β-hydroxybutyrate (PHB) is a promising carbon source for biological mitigation of nitrogen pollution, a significant problem in aquaculture that physical and chemical methods have not provided a comprehensive solution. Here we investigated the impact of PHB on the zero-water-change largemouth bass culture by 30- and 40-day experiments. PHB loaded into the filter circulation pump at 4g L-1, optimum value determined by the first experiment, significantly reduced the levels of nitrate by 99.65%, nitrite by 95.96%, and total nitrogen by 85.22% compared to the control without PHB. PHB also significantly increased denitrifying bacteria (e.g., Proteobacteria and Fusobacteria) and expression of denitrification genes (e.g., nirK and nirS) in the microbial community, improving growth and health parameters of largemouth bass. While the impact may vary in other culture systems, PHB thus demonstrated its remarkable utility in aquaculture, highlighting ecological assessment and application to larger aquaculture operations as future considerations.

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Expression data from NT and PHB siRNA treated hESCs

Project description:Embryonic stem cells (ESCs) are useful resources for clinical cell therapy as its unlimited self- renewal and pluripotecy properties, so it is critical to understand how ESCs maintain its identity. We reported a gene named PHB is essential for hESC self- renewal. We used microarrays to find out the potential mechanisms regulated by PHB in maintaining hESC identity.

2016-11-30 | GSE71765 | GEO

Genes differentially expressed Haloarcula hispanica strains: PHB (M-NM-^TphaEC mutant) vs 960 (wild type)

Project description:Transcriptional profiling of Haloarcula hispanica comparing PHB with 960. PHB represents the PHA synthase genes mutant (i.e., M-NM-^TphaEC) which is deficient in PHBV accumulation when grown in MG medium. 960 represents the wild-type strain which can produce PHBV when grown in MG medium. Goal was to explore the PHBV biosynthesis and its impact on central metabolism in H. hispanica. Total RNA from PHB and 960 were used to generate target cDNA, and then hybridized to 8*15K Haloarcula hispanica genome array genechips, representing about 3800 genes.

2013-01-22 | E-GEOD-42799 | biostudies-arrayexpress

Genes differentially expressed Haloarcula hispanica strains: PHB (ΔphaEC mutant) vs 960 (wild type)

Project description:Transcriptional profiling of Haloarcula hispanica comparing PHB with 960. PHB represents the PHA synthase genes mutant (i.e., ΔphaEC) which is deficient in PHBV accumulation when grown in MG medium. 960 represents the wild-type strain which can produce PHBV when grown in MG medium. Goal was to explore the PHBV biosynthesis and its impact on central metabolism in H. hispanica.

2013-01-22 | GSE42799 | GEO

In vivo disruption of Rb-E2F-Ezh2 signaling loop causes bladder cancer development

Project description:Bladder cancer (BC) is a highly prevalent human disease in which Rb pathway inactivation and epigenetic alterations are common events. However, the connection between these two processes is still poorly understood. Here we show that the in vivo inactivation of all Rb family genes in the mouse urothelium is sufficient to initiate BC development. The characterization of the mouse tumors revealed multiple molecular features of human BC, including the activation of E2F transcription factor and subsequent Ezh2 expression, and the activation of several signaling pathways previously identified as highly relevant in urothelial tumors. Whole transcriptional characterizations of the mouse bladder tumors revealed a significant overlap with human BC samples, and a predominant role for Ezh2 in the downregulation of gene expression programs. Importantly, we determined that in human superficial BC patients, the increased tumor recurrence and progression in these recurrences is associated with increased E2F and Ezh2 expression and Ezh2-mediated gene expression repression. Collectively, our studies provide a genetically defined model for human high-grade superficial BC and demonstrate the existence of an Rb-E2F-Ezh2 axis in bladder whose disruption can promote tumor development. Gene expression was analyzed in normal bladder and bladder tumours, both in humans and in transgenic mice.

2014-10-02 | E-GEOD-38264 | biostudies-arrayexpress

Expression data from bladder tumors and adjacent normal tissues

Project description:miRNAs are involved in cancer development and progression,acting as tumor suppressors or oncogenes. Half of the human miRNAs are located in cancer-associated genomic regions and can function as tumor suppressor genes or oncogenes depending on their targets miRNA profiling was performed on paired bladder cancer tissues and differentially expressed miRNAs were identified in BC and adjacent noncancerous tissues of any disease stage/grade. Ten paired bladder cancer tissues (5 low-grade non-muscle-invasive bladder cancer[NMIBC] and 5 high-grade muscle-invasive bladder cancer[MIBC]) were sent to CapitalBio Corp. (Beijing) for noncoding RNA microarray analysis. The microarray analysis was done as described on the Web site of CapitalBio. NMIBC samples include 07A, 19A, 23A, 24A and T63 while coresponding pairs include 07B, 19B, 23B, 24B and 63. MIBC samples include 10A, 20A, 21A, 34A and 49A while coresponding pairs include 10B, 20B, 21B, 34B and 49B.

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